Resident - American College of Physicians

RESIDENT FELLOW TABLE OF CONTENTS
RESIDENT FELLOW VIGNETTE PODIUM PRESENTATIONS ........................................................................... 68
ARIZONA PODIUM PRESENTATION - CLINICAL VIGNETTE Irbaz Riaz, MD .............................................. 69
Loperamide Induced Cardiac Dysrhythmias – An Emerging Toxicological Phenomenon................... 69
MARYLAND PODIUM PRESENTATION - CLINICAL VIGNETTE Candice Crichlow, MD .............................. 70
Hypertensive Encephalopathy or more? Posterior Reversible Encephalopathy Syndrome and a novel
treatment. ........................................................................................................................................... 70
MASSACHUSETTS PODIUM PRESENTATION - CLINICAL VIGNETTE Fadi Alkhatib, DO ............................ 71
Too little can make you bleed, too much can give you a heart attack! .............................................. 71
MICHIGAN PODIUM PRESENTATION - CLINICAL VIGNETTE Jandark Yuseif, MBchB .............................. 72
Chicken Pox, as the initial presentation of hairy cell leukemia. ......................................................... 72
MINNESOTA PODIUM PRESENTATION - CLINICAL VIGNETTE Jennifer Chang Chieh Yui, MD ................ 73
Serotonin Syndrome in Single Agent Bupropion Overdose ................................................................ 73
NEW YORK PODIUM PRESENTATION - CLINICAL VIGNETTE Dilasha Katwal, MD ................................... 74
West Nile Virus Induced Opsoclonus-Myoclonus Syndrome.............................................................. 74
TEXAS PODIUM PRESENTATION - CLINICAL VIGNETTE Alfredo Camero Jr, MD ..................................... 75
Classic Hypertensive Emergency? An Unusual Case of Labile Hypertension...................................... 75
TEXAS PODIUM PRESENTATION - CLINICAL VIGNETTE Vineet S Gudsoorkar, MBBS ............................. 76
Pay Heed to Weed: It’s a diagnostic lead and a public health need! ................................................. 76
TEXAS PODIUM PRESENTATION - CLINICAL VIGNETTE John Hunninghake, MD .................................... 77
Arterial Thrombus and Myocardial Infarction after Discontinuation of a Novel Oral Anticoagulant in
a Patient with Protein C Deficiency .................................................................................................... 77
[Date]
VIRGINIA PODIUM PRESENTATION - CLINICAL VIGNETTE Nathaniel C Warner, MD .............................. 78
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Look What the Cat Dragged In: An Unusual Case of LVAD-associated Endocarditis. ......................... 78
RESIDENT FELLOW VIGNETTE POSTER FINALSTS ........................................................................................ 79
ALABAMA POSTER FINALIST - CLINICAL VIGNETTE Ashley E Jackson, MD ............................................. 80
Spontaneous native aortic valve thrombosis: a rare case teaches vital medical points .................... 80
ALABAMA POSTER FINALIST - CLINICAL VIGNETTE Sarah R Kunin, MD .................................................. 81
Dying for Moonshine: A rare case of copper toxicity ......................................................................... 81
ARIZONA POSTER FINALIST - CLINICAL VIGNETTE Jawad Bilal, MD ........................................................ 82
Intravenous Immunoglobulin induced pulmonary embolism: It's time to act! .................................. 82
ARIZONA POSTER FINALIST - CLINICAL VIGNETTE Melissa A Crawley, MD............................................. 83
In a Pickle: Foodborne Botulism ......................................................................................................... 83
ARIZONA POSTER FINALIST - CLINICAL VIGNETTE Kyle J Henry, MD ...................................................... 84
Large B Cell Lymphoma presenting as Bilateral Lower Extremity Pain, Asymptomatic Pericarditis and
Pericardial Effusion ............................................................................................................................. 84
ARIZONA POSTER FINALIST - CLINICAL VIGNETTE Edward R Maharam, MD .......................................... 85
Improving Sepsis & Worsening Hypoglycemia? A Case of Levofloxacin Associated Hypoglycemia. .. 85
ARIZONA POSTER FINALIST - CLINICAL VIGNETTE Geoffrey J Orme, DO ................................................ 86
Post-gastric bypass hypoglycemia with bulimia nervosa: An even more frustrating disorder .......... 86
ARIZONA POSTER FINALIST - CLINICAL VIGNETTE Namit N Rohant, MD ................................................ 87
The Ancient Disease Scurvy: A Medical Mystery in the Modern World Secondary to Celiac Disease87
ARKANSAS POSTER FINALIST - CLINICAL VIGNETTE Jorge L Jo Kamimoto, MD ...................................... 88
The Case of the Bound Insulin ............................................................................................................ 88
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Shudhanshu Alishetti, MD ................................... 89
[Date]
Leukemoid Reaction in Extraintestinal Amebiasis .............................................................................. 89
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CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Mekhala Chandra, MD......................................... 90
Catecholamine Induced Peripartum Cardiomyopathy: A Rare Reversible Cause .............................. 90
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Amy L Cummings, MD ......................................... 91
Transplanted, pregnant and in pain: An imaging dilemma in a renal transplant patient with
urosepsis and continued pyuria .......................................................................................................... 91
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Vidhi Doshi, MD ................................................... 92
Malignant Solitary Fibrous Tumor of the Pleura................................................................................. 92
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Masoud Ghaemmaghami .................................... 93
Pulsatile Venous Doppler Waveform of the Lower Extremities with Visible Swirling; a Clue for
Pulmonary Embolism .......................................................................................................................... 93
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Rola Khedraki, MD ............................................... 94
An Atypical Road To Dialysis ............................................................................................................... 94
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Rachel J Klein, MD ............................................... 95
Hepatocellular Carcinoma in a 25 year old man: Are steroids to blame? .......................................... 95
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Chin C Lee, MD .................................................... 96
Rare Valvular Aneurysms Secondary to Infective Endocarditis .......................................................... 96
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE John Brandon Lough, MD .................................... 97
Acute Cholangitis Secondary to Hepatic Hydatid Cyst Disease with Cyst Super-Infection................. 97
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Mehvish Mahmood, MD ..................................... 98
The Great Mimicker- Melioidosis........................................................................................................ 98
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Stephanie Mai, MD .............................................. 99
Bedside Lung Ultrasound in the Diagnosis and Management of Pneumonia in the ICU Setting ....... 99
Pre-workout Caffeine Supplement Induced Cardiac Arrhythmia Leading to Brain Death ............... 100
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CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Nareg Minaskeian, MD ...................................... 100
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CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Sophia Mytrang Nguyen, MD ............................ 101
Wilson Disease Disguised as Drug Induced Liver Injury from Nitrofurantoin................................... 101
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Quan M Nhu, MD, PhD ...................................... 102
Breathless before the (Scorpion) King: Acute eosinophilic pneumonia following scorpion
envenomation ................................................................................................................................... 102
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Jane Park, MD .................................................... 103
Road Tripper Arrives at a Road Block: Managing Acute Submassive Pulmonary Emboli with
Thrombolytic Therapy ....................................................................................................................... 103
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Nicolas D Prionas, MD, PhD............................... 104
Carbapenem Neurotoxicity: A Case Report ...................................................................................... 104
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Kristin E Schwab, MD......................................... 105
When Typical Provokes the Atypical: CMV Triggering an Unusual Presentation of Atypical
Mycobacterium ................................................................................................................................. 105
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Sarthi R Shah, MD .............................................. 106
Battling Influenza: Extra-Corporeal Membrane Oxygenation and an Emerging Role in Influenza
Associated Acute Lung Injury. ........................................................................................................... 106
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Gautam J Shah, MD ........................................... 107
Vasculitic Neuropathy as Initial Presentation of Granulomatosis with Polyangitis (GPA)................ 107
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Bryant W Wilson, MD ........................................ 108
Testicular Tuberculosis: A Rare Presentation of Extra-Pulmonary TB .............................................. 108
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Nicole Barberis, MD............................................ 109
Fact or Factitious ............................................................................................................................... 109
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Cara E Crouch, MD ............................................. 110
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Miriam Freundt, MD........................................... 111
[Date]
Acute hepatitis C infection transmitted by cadaveric bone graft transplantation ........................... 110
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Invasive Rhizopus infection originating from the chest cavity post pneumonectomy ..................... 111
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Miriam IE Freundt, MD ....................................... 112
Amiodarone Desensitization by a Novel Protocol in a Patient with Advanced Biventricular Heart
Failure and Uncontrolled Ventricular Tachycardia ........................................................................... 112
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Kelsi Lacock, MD ................................................. 113
Pulmonary mucormycosis in a diabetic patient: an unusual presentation. ..................................... 113
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Michael Lam, MD ............................................... 114
Recurrent stroke-like symptoms in a patient with recent trigeminal zoster .................................... 114
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Lauren B Miller, MD ........................................... 115
The Metamorphosis: One Tumor’s Tale of Transformation ............................................................. 115
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Tyler Miller, MD.................................................. 116
Systemic Amyloidosis Presenting as Acalculous Cholecystitis .......................................................... 116
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Muthulakshmi Yegappan, MD ............................ 117
TACEred Into Paralysis ...................................................................................................................... 117
CONNECTICUT POSTER FINALIST - CLINICAL VIGNETTE Bhavtosh Dedania, MD .................................. 118
Ulcerating Skin Lesions, Cocaine and Levamisole ............................................................................. 118
CONNECTICUT POSTER FINALIST - CLINICAL VIGNETTE Birinder S Singh, MD ...................................... 119
Anti-NMDA receptor encephalitis: A Potentially Fatal Autoimmune Encephalitis ........................... 119
CONNECTICUT POSTER FINALIST - CLINICAL VIGNETTE Jin Xu, MD ...................................................... 120
Allopurinol-induced Giant Cell Hepatitis........................................................................................... 120
DELAWARE POSTER FINALIST - CLINICAL VIGNETTE Akash N Sethi, DO ............................................... 121
DELAWARE POSTER FINALIST - CLINICAL VIGNETTE Giovanna L Uzelac, MD ....................................... 122
[Date]
It Will Take Your Breath Away - A Case Of Rapidly Progressing Pulmonary Tumor Thrombotic
MIcroangiopathy ............................................................................................................................... 121
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A Case of Ehrlichiosis: Going on A History and a Hunch ................................................................... 122
DISTRICT OF COLUMBIA POSTER FINALIST - CLINICAL VIGNETTE Munaza M Akunjee, MD ................. 123
Barking Up The Wrong Tree: Recurrent Syncopal Episodes as The Presentation of Coronary
Vasospasm ........................................................................................................................................ 123
DISTRICT OF COLUMBIA POSTER FINALIST - CLINICAL VIGNETTE Ahmed Babiker, MBBS.................... 124
Redefining Tropical Pyomyositis: A Case of Pyomyositis of the Pectoralis Major in an
Immunocompetent Adult ................................................................................................................. 124
DISTRICT OF COLUMBIA POSTER FINALIST - CLINICAL VIGNETTE Joseph J Jennings, MD .................... 125
Help! My ACLS Algorithm Isn’t Working! .......................................................................................... 125
DISTRICT OF COLUMBIA POSTER FINALIST - CLINICAL VIGNETTE Myat Soe, MBBS ............................. 126
An Illusion for Pancreatic Cancer: Autoimmune Pancreatitis (AIP) .................................................. 126
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Vivek Choksi, MD .................................................... 127
Eosinophilic Polymyositis: A rare cause of severe rhabdomyolysis in a 22-year -old female........... 127
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Alexandra Gomez Arteaga, MD .............................. 128
Primary bone marrow gray zone lymphoma presenting with leukemic phase and profound
thrombocytopenia ............................................................................................................................ 128
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Brittany McCreery, MD ........................................... 129
A CASE OF VANISHING PLEURAL EFFUSION ...................................................................................... 129
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Jordan C Ray, MD .................................................... 130
Chemical Mediastinitis and Pericarditis Secondary to large Pancreaticopleural-mediastinal Fistula
.......................................................................................................................................................... 130
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Jordan C Ray, MD .................................................... 131
Immune Reconstitution Syndrome in a Patient with Suspected Rheumatoid Arthritis Masking Late
Onset Whipple’s Disease................................................................................................................... 131
Foix- Alajouanine syndrome: A rare and treatable cause of paraplegia........................................... 132
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FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Debjit Saha, MD ...................................................... 132
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FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Wassim Samra, MD ................................................. 133
A new diagnosis of Hemoglobin SC Disease saves a woman’s life ................................................... 133
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Sam Thomas, MD .................................................... 134
A Rare Case of Goblet Cell Carcinoid Tumor Presenting as Small Bowel Obstruction ..................... 134
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Prakhar Vijayvargiya, MD ........................................ 135
Neurocysticercosis presenting as Chronic Relapsing Aseptic Meningitis ......................................... 135
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Danlu Wang, DO...................................................... 136
Myeloid Sarcoma Mimicking Acute Appendicitis as the Initial Presentation of Acute Promyelocytic
Leukemia ........................................................................................................................................... 136
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Mohamad Zetir, MD................................................ 137
Intestinal Angioedema in the Setting of Angiotensin Receptor Blocker Use ................................... 137
GEORGIA POSTER FINALIST - CLINICAL VIGNETTE Daisy Azana, MD .................................................... 138
Hemolytic Uremic Syndrome, a rare manifestation of Clostridium Difficile colitis .......................... 138
GEORGIA POSTER FINALIST - CLINICAL VIGNETTE Mohammed Hasan Khan, MD ................................ 139
Gordonia: Master of Disguise, Cause of Infections ........................................................................... 139
GEORGIA POSTER FINALIST - CLINICAL VIGNETTE CPT David Schmitt, MC USA ................................... 140
Hemoptysis in a Triathlete: A Case of Swimming Induced Pulmonary Edema ................................. 140
GEORGIA POSTER FINALIST - CLINICAL VIGNETTE Kelly D Schrapp, MD............................................... 141
A rare case of Moya Moya disease in an African American male ..................................................... 141
GEORGIA POSTER FINALIST - CLINICAL VIGNETTE Christopher J Walsh, MD ....................................... 142
The Association Between Atrial Fibrillation and Sleep Apnea .......................................................... 142
HAWAII POSTER FINALIST - CLINICAL VIGNETTE Ittikorn Spanuchart, MD ........................................... 143
[Date]
Retrograde Cerebral Venous Air Embolism Secondary to Hepatic Portal Venous Gas .................... 143
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ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Adjoa Anyane-Yeboa, MD........................................ 144
A Case of Black Esophagus After PEA Arrest ..................................................................................... 144
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Anushka Baruah, MD ............................................... 145
An Unusual Case of Liver Abscess: .................................................................................................... 145
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Christopher W Bogan, MD ....................................... 146
Neurosyphilis presenting as bipolar disorder in a young woman..................................................... 146
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Camilo Cano Portillo, MD ........................................ 147
To Drop or Not to Drop: Managing Severe Hypernatremia in the Setting of Hyperosmolar
Hyperglycemic State. ........................................................................................................................ 147
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Samaneh Dowlatshahi, MD ..................................... 148
Thyroid Hormone Resistance: A Case Report ................................................................................... 148
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Samaneh Dowlatshahi, MD ..................................... 149
Successful Treatment of an Acute Hypertriglyceridemia-Induced Pancreatitis Using Insulin and
Heparin Infusion................................................................................................................................ 149
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Amrutha Mary George, MD ..................................... 150
Colistin Induced Hypercapnic Respiratory Failure: Old Drug, Toxicity Revisited .............................. 150
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Baqer Haider, MBBS ................................................ 151
An outlier of inflammatory arthropathy in Coxsackie B infection. ................................................... 151
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Abdalla Hassan, MD ................................................. 152
Rapidly Progressive Multicenteric Castleman’s Disease in Patient with Acute Retroviral Syndrome: A
Case Report ....................................................................................................................................... 152
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Abdalla Hassan, MD ................................................. 153
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Laura N Hernandez, MD .......................................... 154
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Two Lumens-One Artery, Spontaneous Spiral Coronary Artery Dissection in Middle- Age Female
Presenting with Unstable Angina: Case Report ................................................................................ 153
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A case of Strongyloides Hyperinfection leading to diffuse alveolar hemorrhage and appendicitis. 154
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Janet Jang, MD......................................................... 155
Connecting the dots - a case of autoimmune polyglandular syndrome type II ................................ 155
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Sima Kavand, MD ..................................................... 156
Double trouble: A case of DRESS syndrome with overlapping Steven Johnson’s syndrome ........... 156
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Sathish Kumar Krishnan, MD ................................... 157
It Is Not The Plasmodium That Dropped The Counts – A Case Of Hemophagocytic Syndrome....... 157
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Aman Kugasia, MD................................................... 158
Systemic lupus erythematosus, psoriasis, psoriatic arthritis successfully treated with Ustekinumab.
.......................................................................................................................................................... 158
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Mohamad Hani Lababidi, MD .................................. 159
A severe case of Microscopic Polyangitis causing diffuse alveolar hemorrhage and anemia .......... 159
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE John J Lee, MD ......................................................... 160
Beware of Wild cARDS: Blastomycosis.............................................................................................. 160
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Nanditha N Malakkla, MD ....................................... 161
Esophageal Perforation as a Complication of Colonoscopy ............................................................. 161
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Annia M Martial, MD ............................................... 162
Beware of the “SPICE” you get on street .......................................................................................... 162
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Jorge Morales, MD................................................... 163
A rare but life-threatening complication of warfarin therapy: a case of diffuse alveolar hemorrhage.
.......................................................................................................................................................... 163
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Aswin Nukala, MD ................................................... 164
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Tumor Lysis Syndrome as a Complication of Chemoembolization with Irinotecan in a Patient with
Primary Colonic Adenocarcinoma with Liver Metastases ................................................................ 164
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ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Aswin Nukala, MD ................................................... 165
An Unusual Case of Hepatitis C Associated Cryoglobulinemia and Membranoproliferative
Glomerulonephritis Presenting as Diffuse Alveolar Hemorrhage .................................................... 165
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Chibuzo C Odigwe, MD ............................................ 166
Richter’s Transformation of Chronic Lymphocytic Leukemia to Classical Hodgkin Lymphoma ....... 166
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Venu Pararath Gopalakrishnan, MD ........................ 167
Can a Verse (POEM) get any worse!? ............................................................................................... 167
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Siwadon Pitukweerakul, MD ................................... 168
Acute pericarditis as a rare consequence of Severe Diabetic Ketoacidosis...................................... 168
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Siwadon Pitukweerakul, MD ................................... 169
What we have learned from lithium toxicity. ................................................................................... 169
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Moni Roy, MD .......................................................... 170
Carbapenem Resistant Aeromonas Caviae Causing Infected Pancreatic Pseudocyst ...................... 170
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Dhavel Save, MD ...................................................... 171
Alcoholic intoxication leading to Rhabdomyolysis and Bilateral Sub-massive Pulmonary Embolism
.......................................................................................................................................................... 171
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Anushi Shah, MD ..................................................... 172
A Perplexing Cause of Acute Renal Failure in Prostate Cancer ......................................................... 172
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Timothy Shih, DO ..................................................... 173
Sweetheart: A Case of Tricuspid Valve Endocarditis Presenting as Hyperosmolar Hyperglycemic
State (HHS) ........................................................................................................................................ 173
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Nabeel H Siddiqui, MD............................................. 174
May-Thurner Syndrome: A rare cause of Deep Venous Thrombosis ............................................... 174
[Date]
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Simranjit Singh, MD ................................................. 175
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Lung Hamartoma. Is it really a benign pathology? ........................................................................... 175
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Teja V Surapaneni, MD, MS ..................................... 176
Diffuse alveolar hemorrhage (DAH) secondary to amiodarone and apixaban use: A case report ... 176
INDIANA POSTER FINALIST - CLINICAL VIGNETTE Emily Cochard, MD ................................................. 177
Searching for Sarcoid: Utility of PET/CT Scan ................................................................................... 177
INDIANA POSTER FINALIST - CLINICAL VIGNETTE Jinous Etemadi, MD ................................................ 178
A Case of a 30 year old Presenting with a Rare Condition Disguised as B Cell Lymphoma. ............. 178
INDIANA POSTER FINALIST - CLINICAL VIGNETTE Rohan Mehta, MD .................................................. 179
Salmonella isolation from perinephric abscess ................................................................................ 179
INDIANA POSTER FINALIST - CLINICAL VIGNETTE Wesley S Prichard, DO ............................................ 180
Amiodarone-Induced Cirrhosis in the Absence of Long-Standing Transaminase Elevation ............. 180
INDIANA POSTER FINALIST - CLINICAL VIGNETTE Harsh R Shah, DO .................................................... 181
Unlucky 13: A Bleeding Mystery of an 88 year old female ............................................................... 181
IOWA POSTER FINALIST - CLINICAL VIGNETTE Snigdha Jain, MBBS...................................................... 182
EBV Infection in an Immunocompromised Host: When “Mono” is Not Alone ................................ 182
IOWA POSTER FINALIST - CLINICAL VIGNETTE Megan L Srinivas, MD .................................................. 183
Mycophenolate-Induced Disseminated TB in a PPD-Negative Patient ............................................ 183
IOWA POSTER FINALIST - CLINICAL VIGNETTE Maria T Story, MD ....................................................... 184
All That Glitters is not Gold ............................................................................................................... 184
IOWA POSTER FINALIST - CLINICAL VIGNETTE Alexis I Wickersham, MD ............................................. 185
Postpartum Chest Pain and Cardiac Arrest ....................................................................................... 185
Testicular Sarcoidosis ........................................................................................................................ 186
[Date]
KANSAS POSTER FINALIST - CLINICAL VIGNETTE Anjalee Goel Carlson, DO ......................................... 186
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KANSAS POSTER FINALIST - CLINICAL VIGNETTE Kaitlin M Ditch, MD .................................................. 187
STORM IN AN UNSUSPECTING PATIENT ........................................................................................... 187
KANSAS POSTER FINALIST - CLINICAL VIGNETTE Justin G Fernandez, MD ........................................... 188
Undiagnosed Systemic Lupus Erythematous Presenting as Hemophagocytic Lymphohistiocytosis 188
KANSAS POSTER FINALIST - CLINICAL VIGNETTE Rossa Khalaf, MD ..................................................... 189
Multiple Myeloma as Cyclic Vomiting Syndrome ............................................................................. 189
KENTUCKY POSTER FINALIST - CLINICAL VIGNETTE Michael E Jesinger, MD ........................................ 190
TRIPOLAR DISORDER ......................................................................................................................... 190
KENTUCKY POSTER FINALIST - CLINICAL VIGNETTE Justin R Kingery, MD PhD..................................... 191
“You’re Not Dying” and Other Acceptable Lies: Ethical Communication in Global Health .............. 191
LOUISIANA POSTER FINALIST - CLINICAL VIGNETTE Ramsy A Abdelghani, MD .................................... 192
Early Continuous Venovenous Hemodiafiltration in Preventing Permanent Kidney Injury in Severe
Rhabdomyolysis ................................................................................................................................ 192
LOUISIANA POSTER FINALIST - CLINICAL VIGNETTE John B Rhodes Jr, MD .......................................... 193
Arterial Fistulization to the Duodenum as a Complication of Chronic Pancreatitis: A Case Report. 193
LOUISIANA POSTER FINALIST - CLINICAL VIGNETTE Jonathan R Schroeder, MD ................................. 194
Massive Pulmonary Embolism: A rare presentation of Acute HIV-1 Infection ................................. 194
MAINE POSTER FINALIST - CLINICAL VIGNETTE David J Buzanoski, MD ............................................... 195
An Unusual Complication of Crohn’s Disease: Neuro-Enteric Fistula and Gram Negative Rod
Meningitis ......................................................................................................................................... 195
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Selwan Bangean Abdullah, MD .......................... 196
Ependymoma: Surprising Explanation of Neurologic Findings in an untreated SLE patient ............ 196
Acute ischemic stroke secondary to reactive thromobocytosis due to iron deficiency anemia ...... 197
[Date]
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Deepti R Baheti, MBBS ....................................... 197
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MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Stephanie Chen, MD .......................................... 198
A "Tear"-ible Culprit .......................................................................................................................... 198
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Jyotsna Gummadi, MBBS ................................... 199
MEGACOLON IN THE CHEST .............................................................................................................. 199
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Samuel B Holzman, MD ...................................... 200
Bedaquiline, a new weapon in an old war ........................................................................................ 200
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Mohammad Ali Syed Jafri, MD ........................... 201
Acquired Frozen Shoulder: What's the "Factor" ............................................................................... 201
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Amit A Kulkarni, MD ........................................... 202
Untreated Hepatitis C Virus infection presenting with cryoglobulinemic vasculitis and
membranoproliferative glomerulonephritis ..................................................................................... 202
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Ivana Milojevic, MD............................................ 203
Splenic infarcts in a patient with sickle cell trait and recent EBV infection ...................................... 203
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Ivana Milojevic, MD............................................ 204
Have you heard of this bug? Emergence of Leclercia adecarboxylata. ............................................ 204
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Nafees A Mohammed, MBBS ............................. 205
STEMI SECONDARY TO DIC IN THE SETTING OF PNEUMOCOCCAL SEPSIS - A TREATMENT DILEMMA
.......................................................................................................................................................... 205
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Radhika Parikh, MD ............................................ 206
Cryptogenic Organizing Pneumonia Presenting As Recurrent Pneumonia ...................................... 206
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Chintan Pankaj Patel, MD................................... 207
A Clean End ....................................................................................................................................... 207
Embolic stroke: Rare Presentation of Cor Triatriatum...................................................................... 208
[Date]
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Emma Sargsyan, MD .......................................... 208
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MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Dariush Shahsavari, MD ..................................... 210
ZINC-DEFICIENCY ACRODERMATITIS IN A PATIENT WITH CHRONIC ALCOHOLISM AND GASTRIC
BYPASS .............................................................................................................................................. 210
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Eugene Shenderov ............................................. 211
Systemic Lupus Erythematosus Masquerading as Ehrlichiosis. ........................................................ 211
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Ruchita Simoes, MD ........................................... 212
STUCK BETWEEN A GIANT BULLA AND INTRACRANIAL HEMORRHAGE : AN INNOVATIVE SOLUTION
.......................................................................................................................................................... 212
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Gurkeerat Singh, MD .......................................... 213
Cost Saving Method to Treat Loculated Parapneumonic Pleural Effusions. .................................... 213
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Fadi Alkhatib, DO ...................................... 214
Unmasking the Silent Infection!........................................................................................................ 214
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Theodora Anagnosyou, MD ...................... 215
Dasatinib toxicity manifesting as pericardial tamponade................................................................. 215
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Swati Baveja, MD ...................................... 216
Adrenal Apoplexy: An Unusual Cause for Crisis Decision-Making .................................................... 216
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Pooja Chitneni, MD ................................... 217
Not Your Average Case of Diabetic Heart Disease ............................................................................ 217
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Adhirath Doshi, MD .................................. 218
Pseudohypoglycemia- Be careful !.................................................................................................... 218
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE David Edasery, MD.................................... 219
“Now You See It, Now You Don’t” - Cardiac Plasmocytoma with Tamponade ................................ 219
Meloxicam Induced Acute Kidney Injury Presenting as Nephrotic Range Proteinuria ..................... 220
[Date]
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Gunjan Garg .............................................. 220
14
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Samaher Hashim, MD ............................... 221
Kikuchi Fujimoto Disease; Out of Sight and Out of Mind?................................................................ 221
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE SAURABH JOSHI, MD ................................ 222
A Rare Cause of Acute Kidney Injury, Proteinuria and CKD in a Young Patient ................................ 222
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Mariam Lotia, MD ..................................... 223
Plasmapheresis: A Rescue Therapy in Thyroid Storm. ...................................................................... 223
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Lucian M Neville, MD ................................ 224
THE UNFORGIVING TROPONIN LEAK ................................................................................................ 224
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Erin E O'Shea, DO ...................................... 225
An Enemy Returns: CSF Melanomatosis ........................................................................................... 225
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Alexander Adams, MD ......................................... 226
Acute Cholecystitis As Initial Presentation Of Metastatic Lobular Breast Carcinoma ...................... 226
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Sourabh Aggarwal, MBBS .................................... 227
All that looks like “Brugada” is not “Brugada” – Case series of Brugada phenocopy caused by
hyponatremia.................................................................................................................................... 227
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Reem Al-Mahdawi, MD ....................................... 228
Marijuana Induced Biliary Dyskinesia ............................................................................................... 228
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Omar Al-Shuwaykh, MD ...................................... 229
A Patient saved his own life-- A curious case of chest pain: Negative Dobutamine SPECT rMPI ending
up with CABG due to triple vessels disease. ..................................................................................... 229
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Tiba Alwardi, MD ................................................. 230
Familial Occipital Neuralgia; Role of the sodium channels in pathogenesis .................................... 230
A Rare Malignancy with Comorbid Hematologic Disorder ............................................................... 231
[Date]
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Mansoor A Arain, MD .......................................... 231
15
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Nicholas A Battista, MD ....................................... 232
Dysphagia Lusoria: an elusive diagnosis ........................................................................................... 232
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Christopher Begley, DO ....................................... 233
An animal bacterium in the human heart – a case of native valve endocarditis caused by
Staphylococcus simulans in an immunocompetent patient ............................................................. 233
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Abeer A Berry, DO ............................................... 234
Benign Metastasis: An Existing Contradiction .................................................................................. 234
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Suma Chinta, MD ................................................. 235
Don't Be Fooled : Fever, Lymphadenopathy and Neutropenia Does Not Always Equal Malignancy
.......................................................................................................................................................... 235
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Christopher Vittorio Di Felice, MD ...................... 236
Shear stress - a case of microangiopathic hemolytic anemia and thrombocytopenia secondary to
idiopathic pulmonary arterial hypertension ..................................................................................... 236
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Kelly Downey, MD ............................................... 237
Where is That Blood Coming From? And Why? Pseudohemoptysis as Presentation of Acute Human
Immunodeficiency Virus Infection .................................................................................................... 237
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE E. Ethan Ebner, DO .............................................. 238
Minocycline-induced hyperpigmentation of aorta and aortic valve ................................................ 238
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE John Samuel Fleming, DO .................................... 239
Morphea: A rare dermatologic finding that may signal the presence of other autoimmune
conditions.......................................................................................................................................... 239
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Adam Forman, MD .............................................. 240
Managing A Case Of Limbic Encephalitis .......................................................................................... 240
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Ayman Founas, DO .............................................. 241
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Lohit Garg, MD..................................................... 242
[Date]
A Rare Case of Encephalopathy Induced by Metronidazole ............................................................. 241
16
Asymptomatic Colonic Ulceration in an Immunocompromised Patient .......................................... 242
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Jon T Golenbiewski, DO ....................................... 243
Azithromycin-Induced Torsade de Pointes: A Rare but Real Risk ..................................................... 243
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Maulik Govani, MD .............................................. 244
A Rare Case of Recurrent Isolated Sleep Paralysis ............................................................................ 244
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Hamza Hashmi, MD ............................................. 245
'Recognising these signs will save lives'..Classical signs of a catastrophic syndrome ...................... 245
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Khatri C Narayan, MBBS ...................................... 246
A rare and interesting cause of Recurrent Pancreatitis .................................................................... 246
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Adnan Kassier, MD .............................................. 247
Common Variable Immunodeficiency Complicated by a Lymphoproliferative Disorder ................. 247
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Arya Lalithakumari, MBBS ................................... 248
Hyperkalemia : to treat or not to treat? ........................................................................................... 248
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Andrea Landon, DO ............................................. 249
Coexistent Xanthogranulomatous Pyelonephritis and Renal Cell Carcinoma .................................. 249
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Larry McMann, MD.............................................. 250
Idiopathic Occipital Neuralgia a Rare Cause of Debilitating Headache ............................................ 250
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Larry McMann, MD.............................................. 251
A Case of Cervical Manipulation Causing Stroke & Exploring its Biomechanics. .............................. 251
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Talin Nemri, MD................................................... 252
Catastrophic antiphospholipid syndrome following bariatric surgery!! ........................................... 252
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Suraj R Raheja, MD .............................................. 254
[Date]
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Otavio Pereira Rodrigues, MD ............................. 253
17
Acute Thrombocytopenia from Severe Hepatitis C Viremia ............................................................. 254
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Tarun Sharma, MD............................................... 255
UFO: Unidentified Foreign Object Causing Retroperitoneal Abscess ............................................... 255
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Travis Tagami, DO ................................................ 256
Acute Aortic Regurgitation in a Dialysis Patient ............................................................................... 256
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Sunit Y Tolia, DO .................................................. 257
An Unusual Presentation of Malignant Melanoma .......................................................................... 257
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Shrey Velani, MBBS ............................................. 258
Neuromyelitis Optica mimicking stroke ............................................................................................ 258
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Andrew Whipple, DO ........................................... 259
Severe Cholestatic Jaundice from an Unanticipated Diagnosis ........................................................ 259
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Andrew Whipple, DO ........................................... 260
Expanding the Differential Diagnosis for Painless Jaundice ............................................................. 260
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Juraj Zahatnansky, MD ........................................ 261
Peripheral neuropathy as a manifestation of Kikuchi-Fujimoto disease, a rare presentation of a rare
disease. ............................................................................................................................................. 261
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Ashley M. Egan, MD .......................................... 262
A Recurrent Broken Heart ................................................................................................................. 262
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Stanislav Henkin, MD ........................................ 263
Got milk? High fat dairy diet causing severe reversible elevation of LDL-C ..................................... 263
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Thanh Phan Ho, MD .......................................... 264
Renal colic unveiling underlying lymphoma ..................................................................................... 264
[Date]
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Gregory P Kaufman, MD ................................... 265
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Renal failure and nephromegaly manifesting from progressive CLL ................................................ 265
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Hannah C Nordhues, MD .................................. 266
Moans without Stones: A Case of Spontaneous Renal Artery Dissection ........................................ 266
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Kelly M Pennington, MD ................................... 267
Lupus There It Is: Atypical Presentation of Lupus in the Setting of Concomitant Plasmodium
Infection ............................................................................................................................................ 267
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Korosh Sharain, MD .......................................... 268
But, The ANCA is Positive!................................................................................................................. 268
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Alan M Sugrue, MBBCh..................................... 269
Recurrent Spontaneous bilateral pneumothorax with thin walled cavities: A case that leads to the
scalp .................................................................................................................................................. 269
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Cyril Varghese, MD ........................................... 270
Pneumonia Masquerading as a Rash ................................................................................................ 270
MISSISSIPPI POSTER FINALIST - CLINICAL VIGNETTE Lewis W Aldred, MD ........................................... 271
Hypophosphatemia Masquerading as Meningitis ............................................................................ 271
MISSISSIPPI POSTER FINALIST - CLINICAL VIGNETTE Doris K Hansen, MD ........................................... 272
Physiologic Paraspinal masses in a patient with Hemoglobin C Disease .......................................... 272
MISSISSIPPI POSTER FINALIST - CLINICAL VIGNETTE Brandon W Lennep, MD ..................................... 273
Extracorporeal Membrane Oxygenation for Electrical Storm as a Complication of Acute Myocardial
Infarction ........................................................................................................................................... 273
MISSOURI POSTER FINALIST - CLINICAL VIGNETTE Cristina Ipatii, MD ................................................. 274
FINDING "NEO" ................................................................................................................................. 274
NEBRASKA POSTER FINALIST - CLINICAL VIGNETTE Maryam F Gbadamosi-Akindele, MD................... 275
[Date]
Hidden over the counter risk: Omeprazole induced acute interstitial nephritis!............................. 275
19
NEBRASKA POSTER FINALIST - CLINICAL VIGNETTE Rajesh Kunadharaju, MBBS ................................. 276
A Rare Case Of Sarcoidosis Presenting As ARDS And Maculopapular Rash...................................... 276
NEVADA POSTER FINALIST - CLINICAL VIGNETTE Pannaga G Malalur, MD .......................................... 277
Neurotoxicity of High Dose Intrathecal Gadolinium for CT Myelogram ........................................... 277
NEVADA POSTER FINALIST - CLINICAL VIGNETTE Susil Sivaraman, MD ................................................ 278
An Unusual Cause for Left Ventricular Systolic Dysfunction: A Problem with Packing .................... 278
NEW HAMPSHIRE POSTER FINALIST - CLINICAL VIGNETTE Khushboo Shah, MD ................................. 279
Jehovah's Witness with a Triple-Hit: Beta-Thalassemia Trait + Paroxysmal Nocturnal
Hemoglobinuria (PNH) + Chronic Myeloid Leukemia (CML) ............................................................. 279
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Martin Miguel I Amor, MD ................................ 281
AORTICO-LEFT ATRIAL FISTULA: A RARE COMPLICATION OF INFECTIVE ENDOCARDITIS ................ 281
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Anteneh Birru, MD ............................................ 282
Idiopathic thromboembolism and occult malignancy ...................................................................... 282
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Ria D'Souza, MD ................................................ 283
Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis associated with ovarian teratoma: a
challenging diagnosis ........................................................................................................................ 283
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Mufaddal Q Dahodwala, MD ............................ 284
Indolent DRESS Syndrome: The Calm Before The Storm .................................................................. 284
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Joseph DeRose, DO ........................................... 285
Human Granulocytic Anaplasmosis in the Setting of a Hunting Injury ............................................. 285
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Prerna Dogra, MBBS ......................................... 286
DRAMATIC RESPONSE TO INFLIXIMAB IN REFRACTORY NEUROSARCOIDOSIS COMPLICATED BY
CRYPTOCOCCAL MENINGITIS ............................................................................................................ 286
[Date]
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Rishi Handa MD................................................. 287
20
Charcoal Heart - Cardiac Metastasis of Malignant Melanoma ......................................................... 287
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Inga Harbuz-Miller, MD..................................... 288
An obscure presentation of congenital heart defect in a septuagenarian lady. .............................. 288
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Uzma Imran, MD ............................................... 289
Recurrent abdominal pain, a difficult diagnosis of Behcet’s disease ............................................... 289
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Waqas Jehangir, MBBS ..................................... 290
Multi-vessel Spontaneous Coronary Artery Dissection: A Diagnostic Challenge in an Unlikely Setting
.......................................................................................................................................................... 290
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Mohleen Kang, MD ........................................... 291
Spontaneous Hemoperitoneum as an Initial Manifestation of Plasma Cell Leukemia..................... 291
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Niktha Kasinathan, MD ..................................... 292
Pulmonary hypertension induced by hyperthyroidism .................................................................... 292
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Niktha Kasinathan, MD ..................................... 293
Hypercalcemia and rash .................................................................................................................... 293
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Javier A Lopez-Moncayo, MD............................ 294
It’s Supposed to Give You “Wings,” Not a New Heart Valve! ........................................................... 294
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Adaeze Nwosu Iheme, MD................................ 295
Lance-Adams Syndrome: Post- hypoxic myoclonus ......................................................................... 295
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Kunal Manmohan Patel, MD ............................. 296
Dtap-Vaccine Induced Myopericarditis Mimicking ST Elevation Myocardial Infarction ................... 296
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Biplab K Saha, MD ............................................. 297
Cancer related Thrombotic Microangiopathy: A deadly disease...................................................... 297
[Date]
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Aileen P Tlamsa, MD ......................................... 298
21
Blood is Thicker Than Water: Early Plasmapheresis in the Treatment of Severe
Hypertriglyceridemia-Induced Pancreatitis ...................................................................................... 298
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Grace Tseng, MD ............................................... 299
Adult Patent Ductus Arteriosis in Two Siblings : Case Report and Investigation.............................. 299
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Naveen Yellappa, MD ........................................ 300
HOOK(ah)ED Up Pneumocytes ......................................................................................................... 300
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Ping Zhang, MD ................................................. 301
STATIN AND ACQUIRED VITAMIN B12 DEFICIENCY .......................................................................... 301
NEW MEXICO POSTER FINALIST - CLINICAL VIGNETTE Alberto Aguayo-Rico, MD ............................... 302
A close encounter of the mixed kind ................................................................................................ 302
NEW MEXICO POSTER FINALIST - CLINICAL VIGNETTE Christopher D Bailey, DO ................................ 303
Eyes Wide Shut: An Uncommon Presentation of Recurrent Granulomatosis with Polyangiitis ...... 303
NEW MEXICO POSTER FINALIST - CLINICAL VIGNETTE Kristen M Gonzales, MD ................................. 304
Biopsy-Confirmed Renal Injury in a Case of Levamisole-Induced ANCA Vasculitis .......................... 304
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Gyanendra K Acharya, MD .................................. 305
Fatal Non-Hepatic Hyperammonemia in ICU Setting – A Rare but Serious Complication following
Bariatric Surgery................................................................................................................................ 305
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Ashwad Afzal, MD ............................................... 306
Unmasking Autoimmune Pancreatitis from Pancreatic Cancer........................................................ 306
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Ayobami T Akenroye, MBChB MPH .................... 307
Hemophagocytic lymphohistiocytosis (HLH): The Mimicker ............................................................ 307
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Hadeel Alkhairw, MD .......................................... 308
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Erik W Anderson, MD .......................................... 309
[Date]
Neurocysticercosis Presenting With Episodic Headaches ................................................................ 308
22
RS3PE AND THE NEED FOR CANCER WORKUP.................................................................................. 309
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Erik W Anderson, MD .......................................... 310
OBSTRUCTIVE UROPATHY DUE TO A URETEROINGUINAL HERNIA................................................... 310
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Suhaib Ahmad Andrabi, MBBS ............................ 311
Rituximab treatment in severe warm autoimmune hemolytic anemia ........................................... 311
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Leila G. Bumanglag, MD ...................................... 312
Black Esophagus: A Case of Acute Esophageal Necrosis ................................................................... 312
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Leila G. Bumanglag, MD ...................................... 313
Superior Mesenteric Artery Syndrome: A rare cause of small bowel obstruction ........................... 313
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Sameer Chadha, MBBS ........................................ 314
Anomalous Origin of Left Main Coronary Artery from Right Sinus of Valsalva ................................ 314
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Christian M Chiavetta, DO ................................... 315
Sarcoidosis and Immune Reconstitution Inflammatory Syndrome in the Era of Highly Active
Antiretroviral Therapy....................................................................................................................... 315
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Usama Ali Daimee, MD ....................................... 316
Abdominal Pain with Dyslipidemia: Unrelated or Something Sinister?............................................ 316
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Arpita Desai, MBBS.............................................. 317
PROLONGED SURVIVAL WITHOUT SYSTEMIC CHEMOTHERAPY IN A NSCLC PATIENT WITH
PATHOLOGICALLY-CONFIRMED SKELETAL METASTASIS................................................................... 317
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Christine A Garcia, MD ........................................ 318
Carry Me Home: A Curious Case of Tumor-Induced Osteomalacia with Fanconi’s Syndrome ........ 318
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE NANCY GUPTA, MD,MBBS................................... 319
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Hayas Haseer Koya, MD ...................................... 320
[Date]
AUTOIMMUNE HEPATITIS IN ASSOCIATION WITH SOFOSBUVIR AND RIBAVIRIN ............................ 319
23
Unraveling The Mystery Of Neurocutaneous Manifestations In A Young Male............................... 320
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Sandeep S Jubbal, MBBS ..................................... 321
Unusual Presentation of Pulmonary Actinomycosis with 'stem-and-bud' Appearance on CT Scan 321
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Arunpreet S Kahlon, MBBS .................................. 322
LACTATEMIA OF UNKNOWN SIGNIFICANCE IN A PATIENT WITH GLIOBLASTOMA .......................... 322
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Morgan Samuel Kellogg, MD ............................... 323
Chikungunya Virus: An emerging threat? A chronical of the first American death secondary to CHIKV
.......................................................................................................................................................... 323
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Sarah Khan, MD ................................................... 324
Cryptococcocal Meningoencephalitis in a Non-HIV Patient - The Search for an Underlying Disease
.......................................................................................................................................................... 324
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Sunyoung Lee, MD,PhD ....................................... 325
Fulminant hepatic failure from hemophagocytic lymphohistiocytosis secondary to hepatosplenic Tcell lymphoma ................................................................................................................................... 325
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Saurav Luthra, MD,MBBS .................................... 326
A RARE CASE OF HYPERAMMONEMIC ENCEPHALOPATHY SECONDARY TO VALPROATE TOXICITY 326
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Suman Majumdar, MD ........................................ 327
Irreversible Paraplegia in a Systemic Lupus Erythematosus(SLE) Patient ........................................ 327
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Kaushik Mandal, MD ........................................... 328
STEMI of a rarest etiology: an unusual case report .......................................................................... 328
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Jessica J Patel, MD ............................................... 329
Parotid MALToma as the Initial Presentation of Sjogren’s Syndrome.............................................. 329
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Bradley William Petkovich, MD ........................... 330
[Date]
A RARE CAUSE OF REFRACTORY ASCITES - A REMINDER THAT SEEING IS BELIEVING ...................... 330
24
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Darya Rudym, MD ............................................... 331
“All Smoke, no Mirrors”: Pulmonary Langerhans Cell Histiocytosis in Smokers .............................. 331
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Gokul Samudrala, MD ......................................... 332
A RARE CASE OF ACUTE MYOCARDIAL INFARCTION SECONDARY TO CORONARY EMBOLISM IN A
PATIENT WITH NON-ISCHEMIC CARDIOMYOPATHY......................................................................... 332
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Najamus Sehar, MD............................................. 333
Collapsing Focal Segmental Glomerulosclerosis in an HIV negative, Acute Malaria infected patient
.......................................................................................................................................................... 333
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Sumaira Shafi, MD ............................................... 334
DIFFUSE LARGE B CELL LYMPHOMA PRESENTING AS ISOLATED SPLENOMEGALY. .......................... 334
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Yash Shravah, MD ............................................... 335
Smoking - What is it good for? .......................................................................................................... 335
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Pramod Theetha Kariyanna, MD ......................... 336
Myocardial Ischemia following Intracavernosal Phenylephrine Injection for Priapism secondary to
Tamsulosin ........................................................................................................................................ 336
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Sharmila Tilak, MD .............................................. 337
Tell me where you have been so I can tell you what you have ........................................................ 337
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Mazen Zaarour, MD ............................................ 338
MAS: A Can’t Miss!............................................................................................................................ 338
NORTH CAROLINA POSTER FINALIST - CLINICAL VIGNETTE Sean A Marco, MD ................................... 339
Up Against Extremes: The Challenge of Treating Thromboembolism in Obese Patients After Gastric
Bypass ............................................................................................................................................... 339
NORTH CAROLINA POSTER FINALIST - CLINICAL VIGNETTE Samaya J Qureshi, MD ............................. 340
OHIO POSTER FINALIST - CLINICAL VIGNETTE Julia L Agne, MD ........................................................... 341
[Date]
A Triad of Phenazopyridine Toxicity ................................................................................................. 340
25
Empiric Treatment of Cytokine Release Syndrome during Septic Shock .......................................... 341
OHIO POSTER FINALIST - CLINICAL VIGNETTE Amit Arbune, MBBS...................................................... 342
Pyogenic Liver abscess: An Unusual Post-ERCP Complication .......................................................... 342
OHIO POSTER FINALIST - CLINICAL VIGNETTE Matthew R Brown, DO ................................................. 343
E. coli septic arthritis of the shoulder from an unlikely source: a case report ................................. 343
OHIO POSTER FINALIST - CLINICAL VIGNETTE Garren J DeCaro, MD .................................................... 344
Catastrophic Coagulopathy with Thrombocytopenia after Enoxaparin - It’s Not Always Heparin
Induced Thrombocytopenia .............................................................................................................. 344
OHIO POSTER FINALIST - CLINICAL VIGNETTE Mohamed Elrifai, MD ................................................... 345
A peculiar culprit for acute pancreatitis. .......................................................................................... 345
OHIO POSTER FINALIST - CLINICAL VIGNETTE Mohamed Elrifai, MD ................................................... 346
A rare cause of infective endocarditis; Pasteurella multocida infection of the tricuspid valve. ...... 346
OHIO POSTER FINALIST - CLINICAL VIGNETTE Madiha Fida, MBBS ...................................................... 347
Rapidly progressive dyspnea with unexpected autopsy finding ....................................................... 347
OHIO POSTER FINALIST - CLINICAL VIGNETTE Raktim Kumar Ghosh, MD,MBBS ................................. 348
Papulonodular skin lesions with monocytosis: What is your diagnosis? .......................................... 348
OHIO POSTER FINALIST - CLINICAL VIGNETTE Nilamba A Jhala, MD .................................................... 349
Anti-synthetase syndrome associated with cryptogenic organizing pneumonia: Case report and
review of literature. .......................................................................................................................... 349
OHIO POSTER FINALIST - CLINICAL VIGNETTE Sehrish Kamal, MD ....................................................... 350
Guillain Barre Syndrome and Autoimmune Hepatitis...is there a relationship? .............................. 350
OHIO POSTER FINALIST - CLINICAL VIGNETTE Aahd Kubbara, MD ....................................................... 351
OHIO POSTER FINALIST - CLINICAL VIGNETTE Jason V Kunz, DO .......................................................... 352
[Date]
Bilateral Pulmonary Emboli as an Indirect Complication of Gastric Bypass Surgery ........................ 351
26
Levamisole – an Emerging Public Health Threat ............................................................................... 352
OHIO POSTER FINALIST - CLINICAL VIGNETTE Suryanarayan Mohapatra, MD ..................................... 353
A Case of Pituitary Macroadenoma Presenting as Transient Global Amnesia ................................. 353
OHIO POSTER FINALIST - CLINICAL VIGNETTE Ritika Ohri, MD ............................................................. 354
Krokodil-A flesh eating Zombie drug !! ............................................................................................. 354
OHIO POSTER FINALIST - CLINICAL VIGNETTE Brian Petullo, MD ......................................................... 355
Hypoxia after ABVD therapy for Hodgkin’s lymphoma .................................................................... 355
OHIO POSTER FINALIST - CLINICAL VIGNETTE Teresa Ratajczak, MD ................................................... 356
Hemoglobin South Florida a rare Hemoglobin Variant causing falsely elevated HbA1c values. ...... 356
OHIO POSTER FINALIST - CLINICAL VIGNETTE Samantha L Schockman, MD ........................................ 357
Retinal artery occlusion as a first thrombotic event associated with high Factor VIII and low free
protein S in the first trimester of pregnancy .................................................................................... 357
OHIO POSTER FINALIST - CLINICAL VIGNETTE Rupal P Sonani, MBBS .................................................. 358
SPONTANEOUS RETROPERITONEAL BLEEDING DURING HEMODIALYSIS AND A REVIEW OF THE
LITERATURE ....................................................................................................................................... 358
OHIO POSTER FINALIST - CLINICAL VIGNETTE Mohamad Khaled Soufi, MD ........................................ 359
Pneumatosis Intestinalis Including the Left Colon Caused by Ischemic Bowel. ............................... 359
OHIO POSTER FINALIST - CLINICAL VIGNETTE Neetika Srivastava, MD ................................................ 360
Breast Cancer: Rethinking Hormone Receptor Positive (ER+) Disease ............................................. 360
OHIO POSTER FINALIST - CLINICAL VIGNETTE Anandhi Sudhagaran, MD,MBBS .................................. 361
A rare presentation of prostate metastasis to the lung as an isolated lung mass ........................... 361
OHIO POSTER FINALIST - CLINICAL VIGNETTE Erika H Wilson, DO ....................................................... 362
OKLAHOMA POSTER FINALIST - CLINICAL VIGNETTE Omer Iftikhar, MBBS .......................................... 363
[Date]
Seizure with a Surprise...................................................................................................................... 362
27
CLOVES SYNDROME : A case series of three patients with rare overgrowth anomaly. ................... 363
OKLAHOMA POSTER FINALIST - CLINICAL VIGNETTE Kathryn White, DO ............................................ 364
Langerhans Cell Histiocytosis Presenting in an Adult with Mandibular Osteomyelitis .................... 364
ONTARIO POSTER FINALIST - CLINICAL VIGNETTE Siraj Mithoowani, MD ............................................ 365
The blue man: A case of methemoglobinemia secondary to chronic dapsone therapy .................. 365
OREGON POSTER FINALIST - CLINICAL VIGNETTE David M German, MD ............................................. 366
Sympathetic pericarditis? Acute myopericarditis in a patient with concomitant MRSA pneumonia
and empyema ................................................................................................................................... 366
OREGON POSTER FINALIST - CLINICAL VIGNETTE Jia Luo, MD ............................................................. 367
An unusual upper gastrointestinal bleed; Hemobilia as a presentation of chronic portal vein
thrombosis ........................................................................................................................................ 367
OREGON POSTER FINALIST - CLINICAL VIGNETTE Caroline McCulley, MD ........................................... 368
Got Rolaids? A Case of Calcium-Alkali Syndrome ............................................................................. 368
OREGON POSTER FINALIST - CLINICAL VIGNETTE Drew Oehler, MD .................................................... 369
In Defense of the Physical Exam ....................................................................................................... 369
OREGON POSTER FINALIST - CLINICAL VIGNETTE Kevin M Piro, MD .................................................... 370
A Crystal Clear Moment .................................................................................................................... 370
OREGON POSTER FINALIST - CLINICAL VIGNETTE Jennifer Lewis Rosenbaum, MD ............................. 371
Breaking the Spells: Pheochromocytoma as the Initial Presentation of Von Hippel Lindau at Age 80
.......................................................................................................................................................... 371
OREGON POSTER FINALIST - CLINICAL VIGNETTE Amer F Salam, MD .................................................. 372
You Think You Know, But You Don’t Know Behcet’s ........................................................................ 372
OREGON POSTER FINALIST - CLINICAL VIGNETTE David P Serota, MD................................................. 373
[Date]
A Confounding Cavity: The Ellusive Diagnosis of and Invasive Fungal Infection .............................. 373
28
OREGON POSTER FINALIST - CLINICAL VIGNETTE Peter M Smith, MD ................................................. 374
Malaria: A Case That Will Literally Take Your Breath Away .............................................................. 374
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Zohaib Akhtar, MD ....................................... 375
Ovarian Vein Thrombosis: An uncommon cause of abdominal pain which led to a life threatening
complication...................................................................................................................................... 375
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Fuad B Bohsali, MD ...................................... 376
An Anatomic Cause for Progression of Chronic Kidney Disease ....................................................... 376
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Wikrom Chaiwatcharayut, MD .................... 377
Living Diagnosable: Delayed Diagnosis of Cornelia de Lange Syndrome and Devastating Results .. 377
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Wikrom Chaiwatcharayut, MD .................... 378
Not All Myasthenia Gravis Are Created Equal .................................................................................. 378
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Tripti R Chopade, MBBS ............................... 379
Granular cell tumor of common hepatic duct as an unusual cause of jaundice in a patient with acute
hepatitis C: Looking beyond the tip of iceberg! ................................................................................ 379
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Meeta R Desai, MD ...................................... 380
A Rare Cause of Hypercalcemic Crisis: Chronic Myelogenous Leukemia Can Do That? ................... 380
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Beth A Foreman, DO .................................... 381
Novel use of total artificial heart: Terminating refractory arrhythmias in hypertrophic
cardiomyopathy ................................................................................................................................ 381
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Jeydith Gutierrez Perez, MD ........................ 382
A case of unrecognized May-Thurner syndrome leading to recurrent pulmonary embolism ......... 382
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Krithika Krishnarao, DO ................................ 383
COBALT CARDIOMYOPATHY - Blame it on the hips!! ....................................................................... 383
[Date]
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Marvin Louis Roy Lu, MD ............................. 384
29
Aortic Root Abscess without Aortic Valve involvement in an Elderly Male with Diffuse Large B-Cell
Lymphoma presenting with persistent MSSA bacteremia ............................................................... 384
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Marc C Maalouf, MD .................................... 385
A Rare Cause of Heart Failure ........................................................................................................... 385
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Vivek Mehta, MD ......................................... 386
Multiple neoplasms in a patient: Genetic association or coincidence? ........................................... 386
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Vivek Mehta, MD ......................................... 387
CML surfaces after completed course of treatment with Imatinib for gastrointestinal stromal tumor
.......................................................................................................................................................... 387
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Aasim Mohammed, MD ............................... 388
Prinzmetal Angina secondary to Haloperidol: A rare case ............................................................... 388
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Aasim Mohammed, MD ............................... 389
Atypical Hemolytic Uremic Syndrome secondary to Filgrastim: A case report ................................ 389
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Erik W O'Connell, DO ................................... 390
Idiopathic Cardiomyopathy Following Metal-onMetal Hip Arthroplasty: The New Face of "Beer
Drinker's Cardiomyopathy"............................................................................................................... 390
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Temitayo Odesanya, MD.............................. 391
Macrophages Gone Wild................................................................................................................... 391
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Bonnie L Patek, DO ...................................... 392
Refractory Case of Esophageal Web in Male Patient with Alcoholic Liver Disease .......................... 392
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Bonnie L Patek, DO ...................................... 393
A Rare Cutaneous Harbinger of Acute Leukemia: A Case Report ..................................................... 393
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Soumya Patnaik, MD .................................... 394
[Date]
Fighting against all odds- a case of complicated ST elevation myocardial infarction....................... 394
30
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Soumya Patnaik, MD .................................... 395
Levamisole induced vasculitis: is it a relegated diagnostic possibility? ............................................ 395
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Shenthol Sasankan, MD ............................... 396
Imatinib mesylate: a novel treatment option for Bleomycin induced lung injury? .......................... 396
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE LT Jessica L Schwartz, MC USN..................... 397
Primary Hyperaldosteronism: Reassessing a “Negative” Work up ................................................... 397
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Supriya Sekhar, MBBS .................................. 398
LOOK WHAT I FOUND! Coexistent Ehrlichia chaffeensis infection with Klebsiella pneumoniae UTI,
bacteremia and liver abscess. ........................................................................................................... 398
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Madeeha Shams, MD ................................... 399
Fever with rigors following cardiac catheterization – an unusual case of infective endocarditis .... 399
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Sandhya Sharma, MD ................................... 400
A Rare Case of Abdominal Pain due to Spontaneous Isolated Celiac Artery Dissection. ................. 400
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Nawang Sherpa, DO ..................................... 401
Arthroprosthetic Cobaltism Masquerading as Pulmonary Embolism .............................................. 401
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Amber L Sobuto, DO .................................... 402
Borrelia That Takes Your Breath Away ............................................................................................. 402
PENNSYLVANIA POSTER FINALIST - CLINICAL VIGNETTE Zhou Yu, MD................................................. 403
Hemobillia presenting as acute pancreatitis in a patient with hepatocellular carcinoma ............... 403
PUERTO RICO POSTER FINALIST - CLINICAL VIGNETTE Xiomara Cruz, MD ........................................... 404
Unusual cause of Bone Pain .............................................................................................................. 404
PUERTO RICO POSTER FINALIST - CLINICAL VIGNETTE Kilsy A Cuello Pichardo, MD ............................ 405
[Date]
A Rare Cause of Abdominal Pain: Systemic Mastocytosis ................................................................ 405
31
PUERTO RICO POSTER FINALIST - CLINICAL VIGNETTE Amy Lee Gonzalez, MD ................................... 406
Abdominal pain due to perforation: An atypical presentation of Acute Myelogenous Leukemia ... 406
PUERTO RICO POSTER FINALIST - CLINICAL VIGNETTE Jeffrey Maldonado, MD .................................. 407
Atypical Autoimmune Hepatitis in an elderly patient....................................................................... 407
PUERTO RICO POSTER FINALIST - CLINICAL VIGNETTE Hiram Jose Maldonado Quintana, MD ........... 408
MDR TB an Old Disease a Continuous Thread .................................................................................. 408
PUERTO RICO POSTER FINALIST - CLINICAL VIGNETTE Mariely Sanchez, MD ...................................... 409
Aspergillosis in a Hairy Cell Leukemia Patient .................................................................................. 409
RHODE ISLAND POSTER FINALIST - CLINICAL VIGNETTE Nora Hutchinson, MDCM ............................. 410
Lead Astray by Lupus Anticoagulant ................................................................................................. 410
RHODE ISLAND POSTER FINALIST - CLINICAL VIGNETTE Rajesh Shrestha, MBBS ................................. 411
Post-partum hypervagotonia leading to symptomatic sinus bradycardia ........................................ 411
RHODE ISLAND POSTER FINALIST - CLINICAL VIGNETTE Liza Valdivia, MD........................................... 412
Pulmonary Manifestations of Secondary Syphillis: an atypical presentation of the great
masquerader ..................................................................................................................................... 412
RHODE ISLAND POSTER FINALIST - CLINICAL VIGNETTE Nicole B Yang, MD ........................................ 413
New Rash with Ankylosing Spondylitis ............................................................................................. 413
SOUTH CAROLINA POSTER FINALIST - CLINICAL VIGNETTE Sargam Saksena, MD ............................... 414
MYCOBACTERIUM BOVIS SEPTIC ARTHRITIS OF A NATIVE JOINT AFTER TREATMENT WITH INTRAVESICULAR BACILLE CALMETTER-GUERIN (BCG). ............................................................................. 414
SOUTH DAKOTA POSTER FINALIST - CLINICAL VIGNETTE M Azhar Gangat, MD .................................. 415
A Fungal Cause of ARDS In an Immunocompetent Patient .............................................................. 415
The great imitator: What started as a gastroenteritis and ended up as a type I aortic dissection .. 417
[Date]
TENNESSEE POSTER FINALIST - CLINICAL VIGNETTE Smith Giri, MBBS ................................................ 417
32
TENNESSEE POSTER FINALIST - CLINICAL VIGNETTE Victoria Loseva, MD ............................................ 418
Subclavian Steal Syndrome: A rare but important cause of dizziness. ............................................. 418
TENNESSEE POSTER FINALIST - CLINICAL VIGNETTE Poojitha Valasareddy, MD .................................. 419
Macrolipasemia in a 40 year old with SLE: Is it Pancreatitis? ........................................................... 419
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Kongkiat Chaikriangkrai, MD....................................... 420
Successful transcatheter transapical mitral valve-in-valve implantation in an end-stage renal disease
patient ............................................................................................................................................... 420
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Gregory Constantine, MD ........................................... 421
Spontaneous Intra-abdominal Hemorrhage: A Rare Cause of Acute Abdominal Pain ..................... 421
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Crystal Hlaing, MD ...................................................... 422
Leukemia Cutis: an Uncommon Presentation of AML ...................................................................... 422
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Satoko Kanahara, MD ................................................. 423
More than Just a Scar: Violaceous Rash after Liver Transplantation................................................ 423
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Kelvin J Lee, MD .......................................................... 424
From Salt-and-Pepper to Dyspnea and Missed Opportunity – A Case of Rapidly Progressing Systemic
Sclerosis and Rheumatoid Arthritis Overlap Syndrome.................................................................... 424
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Kelvin J Lee, MD .......................................................... 425
Stringing the Liver and Eye: A Case of Near Eye Loss from Klebsiella Pneumoniae ......................... 425
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Pratik Naik, MD ........................................................... 426
The Body Doesn’t Lie! A Case of Pulmonary Foreign Body Granulomatosis. ................................... 426
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Veena A Patel, MD ...................................................... 427
If it isn’t ITP, what could it be? A Confusing Case of Primary Splenic Angiosarcoma ....................... 427
The Warburg effect in the medicine floor ........................................................................................ 428
[Date]
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Alexander Postalian, MD............................................. 428
33
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Quintana Quezada A Raymundo, MD ......................... 429
Exophthalmos – is it always Graves’ disease? .................................................................................. 429
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Juan Remirez, MD ....................................................... 430
A Rare Infectious Complication Secondary To A Left Ventricular Assist Device ............................... 430
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Minal A Shah, MD ....................................................... 431
Too Blue Not to Be True: A Night Float's Diagnostic Dilemma ......................................................... 431
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Andrea M Shioleno, MD.............................................. 432
Mycobacterium Tuberculosis Arthritis Masquerading as a Post-traumatic Joint Effusion .............. 432
TEXAS POSTER FINALIST - CLINICAL VIGNETTE Adil Sulaiman Zahiruddin, MD .................................... 433
Copycat Pancreatitis: A Case of Autoimmune Pancreatitis and the Importance of Early Diagnosis 433
US AIR FORCE POSTER FINALIST - CLINICAL VIGNETTE Matthew Thomas Koroscil, MD ...................... 434
Metastatic melanoma and fever: A case of Clostridium septicum sepsis ........................................ 434
US AIR FORCE POSTER FINALIST - CLINICAL VIGNETTE Ross Pinson, MD ............................................. 435
Two cases of ACE-inhibitor induced visceral angioedema................................................................ 435
US AIR FORCE POSTER FINALIST - CLINICAL VIGNETTE Christopher D Smith, MD................................ 436
Cough Cardioversion of Ventricular Tachycardia.............................................................................. 436
US ARMY POSTER FINALIST - CLINICAL VIGNETTE Ryan Burkhart, DO ................................................. 437
First Case Report: Sildenafil Induced Acute Interstitial Nephritis ..................................................... 437
US ARMY POSTER FINALIST - CLINICAL VIGNETTE CPT Arthur Holtzclaw, MD ..................................... 438
Transfusion Transmitted Malaria Not Preventable by Current Blood Donor Screening Guidelines 438
US ARMY POSTER FINALIST - CLINICAL VIGNETTE CPT Michael J McMahon, MD ................................ 439
[Date]
A DAB OF DANGER: A CASE OF SEVERE RESPIRATORY FAILURE FOLLOWING INHALATION OF
BUTANE HASH OIL ............................................................................................................................. 439
34
US ARMY POSTER FINALIST - CLINICAL VIGNETTE CPT Zorana Mrsic, MD ........................................... 440
Sarcoidosis Related Pleural Effusion Treated with Infliximab Monotherapy ................................... 440
US ARMY POSTER FINALIST - CLINICAL VIGNETTE CPT Cynthia Philip, MD .......................................... 441
A CASE OF SUPPLEMENT-ASSOCIATED ACIDEMIA AND ACUTE KIDNEY INJURY IN AN ACTIVE DUTY
SOLDIER ............................................................................................................................................. 441
US ARMY POSTER FINALIST - CLINICAL VIGNETTE CAPT Bernadette Villarreal, DO ............................. 442
CAPECITABINE INDUCED ARRHYTHMIA ............................................................................................ 442
US NAVY POSTER FINALIST - CLINICAL VIGNETTE LT Clete Barrick, MD ............................................... 443
Hoarse of course: are we underdiagnosing laryngeal Cryptococcus? .............................................. 443
US NAVY POSTER FINALIST - CLINICAL VIGNETTE LT Amie L Harvey, MD............................................. 444
Why is my Hyperparathyroid Patient Itching? .................................................................................. 444
US NAVY POSTER FINALIST - CLINICAL VIGNETTE Dani Leary, DO ........................................................ 445
Life-Threatening Complications from a Life-Saving Device .............................................................. 445
US NAVY POSTER FINALIST - CLINICAL VIGNETTE LT Brennan J Shutt, MC USN ................................... 446
Percutaneous and Invasive Management of a Rare Congenital Pulmonary Malformation in an Active
Duty Service Member ....................................................................................................................... 446
UTAH POSTER FINALIST - CLINICAL VIGNETTE Craig D Robison, MD .................................................... 447
I Have Walked 10,000 Miles and I Will Walk 10,000 More............................................................... 447
VERMONT POSTER FINALIST - CLINICAL VIGNETTE Jonathan B Halevy, MD ........................................ 448
An Infectious Case of Tricuspid Stenosis........................................................................................... 448
VERMONT POSTER FINALIST - CLINICAL VIGNETTE Sherrie Khadanga, MD ......................................... 449
Oozing all over: An interesting case of Acquired Hemophilia A ....................................................... 449
Delayed HHV-6 encephalitis in an allogeneic stem cell transplant patient. ..................................... 450
[Date]
VERMONT POSTER FINALIST - CLINICAL VIGNETTE Jacqueline O'Toole, DO ........................................ 450
35
VERMONT POSTER FINALIST - CLINICAL VIGNETTE Tara Scribner-Metcalf, MD................................... 451
Zebra Spotting: A Case of Adult onset Urea Cycle Disorder ............................................................. 451
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Suliman M Alamro, MD .......................................... 452
An Uncommon Cause of Altered Mental Status ............................................................................... 452
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Maram Alkhatib, MBBCH ....................................... 453
Rabies contracted from a cadaveric renal transplant ....................................................................... 453
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Malik A Anjum, MD ................................................ 454
Loin Pain Hematuria Syndrome (LPHS) ............................................................................................. 454
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Faisal Anwar, MD ................................................... 455
“EVANS” TO BETSY! HOW TO HANDLE THE DELICATE BALANCE BETWEEN THROMBOSIS AND
HEMORRHAGE IN A PATIENT WITH EVANS SYNDROME................................................................... 455
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Christian Bergman, MD .......................................... 456
Rickettsia Parkeri – A headache of a diagnosis ................................................................................. 456
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Jennifer L Copare, DO............................................. 457
Shearing the Pentad: An atypical case of TTP ................................................................................... 457
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Joshua G Gazo, MD ................................................ 458
A lesson in hypocalcemia .................................................................................................................. 458
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Vinay M Gidwani, MD ............................................ 459
MONTELUKAST TO THE RESCUE?...................................................................................................... 459
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Puneet Gill, MD ...................................................... 460
A Rare Case of Acute-Onset Chorea Related to End-Stage Renal Disease ....................................... 460
Relapsing neuroleptic malignant syndrome in a middle aged female previously taking
trifluoperazine and venlafaxine. ....................................................................................................... 461
[Date]
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Michael Y Kim, MD ................................................. 461
36
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE David A Klimpl, MD ................................................ 462
Nacho Average Rash: Sweet’s Syndrome Presenting with Oral and Cutaneous Pathergy ............... 462
First Author: David A Klimpl, MD ...................................................................................................... 462
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Abhishek Nandan, MD ........................................... 463
The Unusual Seed of Strep Mitis ....................................................................................................... 463
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Mayssam A Nehme, MD......................................... 464
Recurrent benign lymphocytic meningitis - A case report................................................................ 464
VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Jeffrey M Sturek, MD, PhD ..................................... 465
Haemophilus Influenzae Biotype VI Cellulitis Resulting in Septic Shock with Multiple Organ
Dysfunction Syndrome ...................................................................................................................... 465
WASHINGTON POSTER FINALIST - CLINICAL VIGNETTE Lindsay A Collins, MD .................................... 466
DRESS: A Deadly Rash ....................................................................................................................... 466
WASHINGTON POSTER FINALIST - CLINICAL VIGNETTE Rachel P Safran, MD ...................................... 467
TESTOSTERONE SUPPLEMENTS: HARDLY A STROKE OF GENIUS ...................................................... 467
WEST VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Grace Y Liu, MD ............................................ 468
Removal of vancomycin in a patient with acute kidney injury using high flux hemodialysis
membranes ....................................................................................................................................... 468
WEST VIRGINIA POSTER FINALIST - CLINICAL VIGNETTE Mehran Moradi, DO ..................................... 469
Should I give Lactulose in Depakote overdose?................................................................................ 469
WISCONSIN POSTER FINALIST - CLINICAL VIGNETTE Grant Boschult, MD ........................................... 470
A “CRYSTAL” Clear Case of Pulmonary Foreign Body Granulomatosis ............................................. 470
WISCONSIN POSTER FINALIST - CLINICAL VIGNETTE Richard L Martin III, MD ..................................... 471
WISCONSIN POSTER FINALIST - CLINICAL VIGNETTE Sarang Patel, MD ............................................... 472
[Date]
Hemolytic Uremic Syndrome (HUS) Presenting in an Adult Chemotherapy Patient ........................ 471
37
ACQUIRED ANGIOEDEMA IN A PATIENT WITH A HISTORY OF CLL ................................................... 472
WISCONSIN POSTER FINALIST - CLINICAL VIGNETTE Sridevi Ramalingam, MD .................................... 473
Preventing Iatrogenic harm by utilizing a collaborative multi-disciplinary multi-modal approach to
managing cancer-related bone pain ................................................................................................. 473
WISCONSIN POSTER FINALIST - CLINICAL VIGNETTE Ruthanna Seidel, MD ......................................... 474
A SELF-LIMITED VIRUS TURNED DEADLY: ADENOVIRUS PNEUMONIA IN A HEALTHY YOUNG ADULT
.......................................................................................................................................................... 474
PODIUM PRESENTATIONS......................................................................................................................... 476
COLORADO PODIUM PRESENTATION - RESEARCH Ryan Daniel Murphy, MD ..................................... 477
IMPLEMENTATION OF A “FOUR C’S” REAL-TIME FEEDBACK TOOL TO ASSESS PATIENT SATISFACTION
AND PROVIDER COMMUNICATION .................................................................................................. 477
ILLINOIS PODIUM PRESENTATION - RESEARCH Abdalla Hassan, MD ................................................... 479
Vascular Closure Device Malfunction: What are we missing? .......................................................... 479
MICHIGAN PODIUM PRESENTATION - RESEARCH Daniel E Ezekwudo, MD ......................................... 480
Methyl Jasmonate: A plant stress hormone that enhances radio-sensitivity of hormone refractory
prostate cancer cells. ........................................................................................................................ 480
MICHIGAN PODIUM PRESENTATION - RESEARCH Suwen Kumar ......................................................... 481
Positive airway pressure affects cardiac remodeling in hypertrophic cardiomyopathy patients with
obstructive sleep apnea .................................................................................................................... 481
NEW JERSEY PODIUM PRESENTATION - RESEARCH Martin Miguel I Amor, MD .................................. 482
IMPROVED EFFICIENCY AND COST SAVINGS FROM TRIAGING SELECTED TRANSIENT ISCHEMIC
ATTACK PATIENTS TO OUTPATIENT URGENT CARE .......................................................................... 482
OHIO PODIUM PRESENTATION - RESEARCH Mahesh Bavineni, MD .................................................... 483
“NOTE BLOAT SYNDROME”: AN EPIDEMIC AFFECTING ELECTRONIC HEALTH RECORDS, HIGH TIME
TO CHANGE SOAP NOTE TO APSO NOTE. ......................................................................................... 483
[Date]
PENNSYLVANIA PODIUM PRESENTATION - RESEARCH Marvin Louis Roy Lu, MD ............................... 484
38
Electrocardiographic Changes Consistent with Atrial Infarction are an Independent Predictor of 30
Day and 1 Year Mortality in Patients with Acute ST-Elevation Myocardial Infarction ..................... 484
PENNSYLVANIA PODIUM PRESENTATION - RESEARCH Loheetha Ragupathi, MD ............................... 485
Proton Pump Inhibitors and Hypomagnesemia in Patients with Arrhythmias ................................. 485
QUEBEC PODIUM PRESENTATION - RESEARCH Catherine Matte, MD ................................................. 486
Improving Prescribing Practices on Clinical Teaching Units: Glucocorticoid Use in Chronic
Obstructive Pulmonary Disease Exacerbations ................................................................................ 486
VIRGINIA PODIUM PRESENTATION - RESEARCH John Smirniotopoulos, MD ....................................... 487
In-hospital cost analysis of Prostate Artery Embolization (PAE) and Transurethral Resection of the
Prostate (TURP) in the treatment of Benign Prostatic Hyperplasia. ................................................. 487
POSTER FINALISTS ..................................................................................................................................... 489
ARIZONA POSTER FINALIST - RESEARCH Adebisi Alli, DO ..................................................................... 490
Innovations in Patient Safety Education of Internal Medicine Residents......................................... 490
CALIFORNIA POSTER FINALIST - RESEARCH Alan Beneze, MD .............................................................. 491
Simplified Pulmonary Embolism Severity Index Accurately Reflects Length of Stay, Readmission and
Death in a California Cohort.............................................................................................................. 491
CALIFORNIA POSTER FINALIST - RESEARCH Seth Blumberg, MD, PhD ................................................. 492
Evaluating the risk of re-emergence of measles in the United States .............................................. 492
CALIFORNIA POSTER FINALIST - RESEARCH Brittany A Doremus, DO................................................... 493
Frequent Premature Atrial Complexes and their Association with Risk of Incident Heart Failure,
Stroke, and All-Cause Mortality. ....................................................................................................... 493
CALIFORNIA POSTER FINALIST - RESEARCH Heather Hofmann, MD .................................................... 495
Teaching on Rounds: Observations, Perceptions, and an Intervention to Increase Bedside Teaching
.......................................................................................................................................................... 495
SOLUBLE GUANYLATE CYCLASE AS A NOVEL TREATMENT TARGET FOR OSTEOPOROSIS ................. 496
[Date]
CALIFORNIA POSTER FINALIST - RESEARCH Jisha K Joshua, MD ........................................................... 496
39
CALIFORNIA POSTER FINALIST - RESEARCH Lucy Liu, MD ..................................................................... 497
Racial Ethnic Differences in Hip Fracture Incidence and Mortality in Older Men ............................ 497
CALIFORNIA POSTER FINALIST - RESEARCH Mala C Mandyam, MD ..................................................... 498
Discharge checklists may reduce medical errors. ............................................................................. 498
CALIFORNIA POSTER FINALIST - RESEARCH Sajan Patel, MD ................................................................ 499
Appropriate Utilization of Telemetry ................................................................................................ 499
CALIFORNIA POSTER FINALIST - RESEARCH Ray Pillai, MD ................................................................... 500
Change in Pulse Oximetry Waveform Before and After Hemodialysis and Ultrafiltration in Critically
Ill Patients May Reflect Hemodynamics ........................................................................................... 500
CALIFORNIA POSTER FINALIST - RESEARCH Veronica Ramirez, MD ..................................................... 501
Health in one touch: Assessing the use of mobile health information by patients of LAC+USC
Medical Center Primary Care Clinics ................................................................................................. 501
CALIFORNIA POSTER FINALIST - RESEARCH Linnaea Schuttner, MD .................................................... 502
The MyCare pilot: Improving non-urgent ED utilization and inpatient admission through ambulatory
multidisciplinary care ........................................................................................................................ 502
CALIFORNIA POSTER FINALIST - RESEARCH Sarthi R Shah, MD ............................................................ 503
Utilization of G Charts to Analyze Rare Occurrence Events in Health Care Quality Improvement .. 503
CALIFORNIA POSTER FINALIST - RESEARCH Viet Tran, DO .................................................................... 504
Percentage of Patients with Gram Positive Bacteremia, Meningitis,Hospital-Acquired Pneumonia,
Severe Sepsis, or Septic Shock who Achieve a Therapeutic First Vancomycin Trough .................... 504
COLORADO POSTER FINALIST - RESEARCH Claudia Ihm, MD ............................................................... 505
Clinical characteristics of patients diagnosed with community-associated Clostridium difficile
infection ............................................................................................................................................ 505
Evaluation of the Appropriate Use and Safety of Intravenous Levothyroxine at an Academic Medical
Center................................................................................................................................................ 506
[Date]
COLORADO POSTER FINALIST - RESEARCH Kara R Mizokami-Stout, MD.............................................. 506
40
CONNECTICUT POSTER FINALIST - RESEARCH Theo Borgovan, MD ..................................................... 507
The Role of Cancer Stem Cells in Gauging Follicular Lymphoma Prognosis ..................................... 507
CONNECTICUT POSTER FINALIST - RESEARCH Kofi M Osei, MD ........................................................... 508
The impact of an awareness campaign on hospital cost reduction and redundant laboratory testing
in a community teaching hospital ..................................................................................................... 508
DELAWARE POSTER FINALIST - RESEARCH Nirmol Philip, MD .............................................................. 510
Supersize This - Improving Resident Communication about Obesity in the Outpatient Clinic ........ 510
DELAWARE POSTER FINALIST - RESEARCH Xian Qiao, MD ................................................................... 512
Reflex to Urine Culture: Truncating the Time Taken to Transport the Tinkle to the Testing ........... 512
FLORIDA POSTER FINALIST - RESEARCH Lucas A Burke, MD ................................................................. 513
Positive predictive value of elevated troponin for diagnosis of acute coronary syndrome ............. 513
FLORIDA POSTER FINALIST - RESEARCH Maroun Sfeir, MD .................................................................. 514
Clinical Laboratory Practices in Speciating Organisms and Reporting Results of Voided Urine
Cultures ............................................................................................................................................. 514
GEORGIA POSTER FINALIST - RESEARCH Salim Hayek, MD .................................................................. 516
College Education is an Independent Predictor of Survival in Patients with Heart Disease or
Cardiovascular Risk Factors Who Undergo Left Heart Catheterization ............................................ 516
GEORGIA POSTER FINALIST - RESEARCH Anthony S Otekeiwebia, MBBS............................................. 517
Performance of Oxygen Saturation Index in Adults with Type 1 Respiratory Failure ...................... 517
GEORGIA POSTER FINALIST - RESEARCH Ayman Samman Tahhan, MD ............................................... 518
Circulating progenitor cells are an independent predictor of coronary artery disease progression 518
HAWAII POSTER FINALIST - RESEARCH Pamela Sebastian, MD, MBBS................................................. 519
ILLINOIS POSTER FINALIST - RESEARCH Pakhadi H Buddhadev, MBBS ................................................. 520
[Date]
Provider Orders for Life-Sustaining Treatment (POLST) Implementation and Training in Nursing
Facilities in Hawaii ............................................................................................................................. 519
41
Correlation between Blood Glucose levels and duration of Mechanical Ventilation....................... 520
ILLINOIS POSTER FINALIST - RESEARCH Briana T Costello, MD ............................................................. 521
IF YOUR PATIENT HAS-BLED, DID YOU CALCULATE THE CHA2DS2-VASc SCORE? ............................ 521
ILLINOIS POSTER FINALIST - RESEARCH Manjusha Das, MD ................................................................. 522
Antibiogram of VRE causing Urinary Tract Infections as a retrospective study from MMC, Springfield
Illinois ................................................................................................................................................ 522
ILLINOIS POSTER FINALIST - RESEARCH Lindsay M Esch, MD ............................................................... 523
Preparing for the Primary Care Clinic: An Ambulatory Boot Camp for Internal Medicine Interns... 523
ILLINOIS POSTER FINALIST - RESEARCH Adriana G Olariu, MD ............................................................. 524
Risk of Crohn’s Disease Recurrence after Surgical Resection: Implications of Tobacco Use and
Preoperative Corticosteroids ............................................................................................................ 524
ILLINOIS POSTER FINALIST - RESEARCH Karthik Ragunathan, MD ........................................................ 525
Rates of infection for single vs multilumen peripherally inserted central catheter: A systematic
review................................................................................................................................................ 525
INDIANA POSTER FINALIST - RESEARCH Emily Cochard, MD ................................................................ 527
Impact of Evidence-Based Guidelines for Management of Clostridium Difficile Infection .............. 527
INDIANA POSTER FINALIST - RESEARCH Stephanie N Martin, MD ....................................................... 528
Evaluation of discrepancies in statin use recommendations between ATP3 and ACC/AHA lipid
guidelines in a primary care population ........................................................................................... 528
INDIANA POSTER FINALIST - RESEARCH Stephen Schutzman, MD ....................................................... 529
The Cost of A Cardiac Marker:It’s Enough to Give You Chest Pain ................................................... 529
IOWA POSTER FINALIST - RESEARCH Chad C Ward, MD ....................................................................... 530
DETECTION OF ARRHYTHMIC EVENTS: AN ASSESSMENT OF SCREENING ........................................ 530
Effects of Revised Consultation Room Design on Patient-Physician Communication ...................... 531
[Date]
KANSAS POSTER FINALIST - RESEARCH Allison J Baughman, MD ......................................................... 531
42
KANSAS POSTER FINALIST - RESEARCH Kaitlin M Ditch, MD ................................................................ 532
Barriers to Enter Weight Maintenance ............................................................................................. 532
KANSAS POSTER FINALIST - RESEARCH Youness Hussein, MD ............................................................. 533
IMPROVING ANTICOAGULATION MANAGEMENT ............................................................................ 533
KANSAS POSTER FINALIST - RESEARCH Mohinder Reddy Vindhyal, MD .............................................. 535
Cardio-Renal association for heart failure re-admissions ................................................................. 535
KENTUCKY POSTER FINALIST - RESEARCH Anub G John, MD................................................................ 536
Changes in Glomerular Filtration Rate (GFR) following implantation of Continuous Flow Left
Ventricular Assist Devices (LVAD) ..................................................................................................... 536
LOUISIANA POSTER FINALIST - RESEARCH Aman Chauhan, MBBS ....................................................... 538
Does the addition of adjuvant intraoperative post-dissection tumor bed chemotherapy during GI
neuroendocrine tumor debulking benefit patients? ........................................................................ 538
MARYLAND POSTER FINALIST - RESEARCH Paul E Miller II, MD ........................................................... 539
HIV and Coronary Arterial Remodeling from the Multicenter AIDS Cohort Study (MACS) .............. 539
MASSACHUSETTS POSTER FINALIST - RESEARCH Fadi Alkhatib, DO..................................................... 540
Long Eye Lashes, and Too long To See Them! .................................................................................. 540
MASSACHUSETTS POSTER FINALIST - RESEARCH Theodora Anagnostou, MD ..................................... 541
The effects of Candida Colonization and antifungal use on the outcomes of patients with VentilatorAssociated Pneumonia ...................................................................................................................... 541
MASSACHUSETTS POSTER FINALIST - RESEARCH Hari Pokharel, MD ................................................... 542
The Baystate Frailty Study – Prevalence of Frailty in a Cohort of Hospitalized Elderly Patients ...... 542
MASSACHUSETTS POSTER FINALIST - RESEARCH Zirui Song, MD ......................................................... 543
MEXICO - POSTER FINALIST - RESEARCH Sonia Rodriguez, MD ............................................................ 544
[Date]
Changes in Health Care Spending and Quality 4 Years into Global Payment for Accountable Care
Organizations .................................................................................................................................... 543
43
Prevalence of pathology renal findings not associated to disease activity in patients with Systemic
Lupus Erythematosus (SLE). .............................................................................................................. 544
MEXICO - POSTER FINALIST - RESEARCH Jorge Rafael Romo Tena, MD ............................................... 545
The E3 ligase Casitas B Lineage Lymphoma b (Cbl-b) Modulates Peripheral Regulatory T cell
Function via p27kip1 in patients with Systemic Lupus Erythematosus. ........................................... 545
MICHIGAN POSTER FINALIST - RESEARCH Sourabh Aggarwal, MBBS................................................... 546
Epidemiology of Takotsubo cardiomyopathy in US: An analysis of NIS data ................................... 546
MICHIGAN POSTER FINALIST - RESEARCH Daniel E Ezekwudo, MD ..................................................... 547
Chapter Winning Abstract................................................................................................................. 547
MICHIGAN POSTER FINALIST - RESEARCH Timothy A Joseph, MD ....................................................... 548
Cost of Mediterranean Diet Compared to Dietary Expenditures Recommended by the United States
Department of Agriculture................................................................................................................ 548
MICHIGAN POSTER FINALIST - RESEARCH Devin Birsingh Malik, MD ................................................... 549
How did the United States Preventative Services Task Force 2005 Guidelines for Abdominal Aortic
Aneurysm Screening Affect Mortality in the United States Population? ......................................... 549
MINNESOTA POSTER FINALIST - RESEARCH Vidhu Anand, MBBS ........................................................ 550
Ofatumumab for Rheumatoid Arthritis: A Cochrane Systematic Review and Meta-analysis .......... 550
MINNESOTA POSTER FINALIST - RESEARCH Joel D Beachey, MD ......................................................... 552
Reducing Unnecessary Routine Lab Tests for Hospitalized Medical Patients .................................. 552
MINNESOTA POSTER FINALIST - RESEARCH Thoetchai Peeraphatdit, MD ........................................... 553
The Relationship between Serum Electrolytes and Electrocardiographic Intervals ......................... 553
MINNESOTA POSTER FINALIST - RESEARCH Paolo Strati, MD .............................................................. 554
Renal Complications of Chronic Lymphocytic Leukemia/Monoclonal B-cell Lymphocytosis (CLL/MBL)
.......................................................................................................................................................... 554
[Date]
MINNESOTA POSTER FINALIST - RESEARCH Priya Vijayvargiya, MD..................................................... 555
44
Characterization of hypothalamic hunger and satiety signals with pulsed arterial spin labeling MRI
.......................................................................................................................................................... 555
MISSISSIPPI POSTER FINALIST - RESEARCH Ben Horton, MD ................................................................ 557
Analysis of a Guideline-Derived Resident Educational Program on Inpatient Glycemic Control ..... 557
MISSISSIPPI POSTER FINALIST - RESEARCH Arnaldo F Lopez-Ruiz, MD................................................. 558
Protective Role of Acute Testosterone Infusion during Acute Kidney Injury (AKI)........................... 558
MISSOURI POSTER FINALIST - RESEARCH Purvi G Patel, MD ................................................................ 559
Incorporation of the 2013 ACC/AHA Lipid Guidelines into the Management of Patients with
Diabetes ............................................................................................................................................ 559
MISSOURI POSTER FINALIST - RESEARCH Dhivya Sugumar, MBBS ....................................................... 561
Improving documentation of Advance Directives and Code status in the outpatient setting by
Resident Physicians ........................................................................................................................... 561
MISSOURI POSTER FINALIST - RESEARCH Li Zhou, MD ......................................................................... 562
Extracorporeal photopheresis as second-line treatment for acute graft-versus-host disease: Impact
on six month freedom from treatment failure ................................................................................. 562
NEVADA POSTER FINALIST - RESEARCH Amhoud Farooq, MBBS ......................................................... 563
Unexpected effects of amino acids and NMDA receptor in the treatment of Acute liver failure and
acetaminophen hepatotoxicity. ........................................................................................................ 563
NEVADA POSTER FINALIST - RESEARCH Shahrukh Hussain Khan, MBBS .............................................. 564
Practices and Utilization of DVT Prophylaxis at a Community Hospital ........................................... 564
NEW JERSEY POSTER FINALIST - RESEARCH Abhinav Agrawal, MD ...................................................... 565
Are we being an Oxy-moron : The overuse of oxygen in a community hospital setting. ................. 565
NEW JERSEY POSTER FINALIST - RESEARCH Abhinav Agrawal, MD ...................................................... 566
Monmouth Emergency Evaluation Tool ( MEET) - a unique tool to predict observation status. ..... 566
Association of Obstructive Sleep Apnea and Pulmonary Hypertension: a meta-analysis ................ 567
[Date]
NEW JERSEY POSTER FINALIST - RESEARCH Tasnim Imran, MD ........................................................... 567
45
NEW JERSEY POSTER FINALIST - RESEARCH Nara Lee, MD ................................................................... 568
Peritoneal Carcinomatosis in Colorectal Cancer: Proposed Algorithm for Cytoreduction/HIPEC .... 568
NEW JERSEY POSTER FINALIST - RESEARCH Abdul Hameed Zaid, MBBS .............................................. 569
Interprofessional education: establishing a collaborative medicine-pharmacy research program. 569
NEW MEXICO POSTER FINALIST - RESEARCH Christopher Bunn, DO ................................................... 571
Improving the Documentation of Nutritional Supplements in an Outpatient Primary Care Clinic .. 571
NEW MEXICO POSTER FINALIST - RESEARCH Benjamin R Deaton, MD ............................................... 572
Trajectory and Long Term Outcomes in Patients with MRSA bacteremia ....................................... 572
NEW YORK POSTER FINALIST - RESEARCH Puvanalingam Ayyadurai, MBBS ........................................ 573
HIV ASSOCIATED PULMONARY ARTERIAL HYPERTENSION IN A COHORT OF HIV INFECTED AFRICAN
AMERICANS. ...................................................................................................................................... 573
NEW YORK POSTER FINALIST - RESEARCH Amit Bhanvadia, MD .......................................................... 574
Shifts in the Microbiota Following Antibiotic Therapy for Clostridium difficile Infection Favor
Enterobacteriaceae ........................................................................................................................... 574
NEW YORK POSTER FINALIST - RESEARCH Sunny Goel, MD ................................................................. 575
Relationship of Body Mass Index With All-Cause and Cardiovascular Mortality and Hospitalizations
in Patients with Chronic Heart Failure- "The Obesity Paradox" ....................................................... 575
NEW YORK POSTER FINALIST - RESEARCH Huijuan Liao, MD ............................................................... 576
The Etiology and Risk Factor Analysis in Hypercalcemic Crisis ......................................................... 576
NEW YORK POSTER FINALIST - RESEARCH Ronald A Luna, MD ............................................................ 577
Patient satisfaction: Is it linked to quality and cost of care? ............................................................ 577
NEW YORK POSTER FINALIST - RESEARCH Naoki Misumida, MD ......................................................... 578
NEW YORK POSTER FINALIST - RESEARCH Amer Nazir, MD, MBBS ...................................................... 579
[Date]
Absence of ST Elevation in Lead V1 Predicts Worse Long-term Outcomes in Patients with First
Anterior ST Elevation Myocardial Infarction ..................................................................................... 578
46
Indwelling Urinary Catheters in Hospitalized Patients: Appropriate Use, Discontinuation and Followup: A Quality Improvement (QI) Project ........................................................................................... 579
NEW YORK POSTER FINALIST - RESEARCH Alejandro Recio Boiles, MD ............................................... 580
Evaluation of a Practical Low-Cost Quality Intervention to Improve Adherence to Evidence-Based
Cancer Screening Recommendations in 642 Patients ...................................................................... 580
NEW YORK POSTER FINALIST - RESEARCH Daniel C Rodriguez, MD ..................................................... 581
Is echocardiogram and left ventriculography both necessary in patients undergoing elective left
heart catheterization? ...................................................................................................................... 581
NEW YORK POSTER FINALIST - RESEARCH Naveen Sablani, MD........................................................... 582
Does an Upright T Wave in Lead V1 Predict Left Anterior Descending Artery Lesion and/or a Left
Circumflex Artery Lesion on Cardiac Catheterization? ..................................................................... 582
NEW YORK POSTER FINALIST - RESEARCH Anawin Sanguankeo, MD ................................................... 583
Association Between NSAIDs and Clostridium difficile-associated Diarrhea (CDAD): a Systematic
Review and Meta-Analysis ................................................................................................................ 583
NEW YORK POSTER FINALIST - RESEARCH Ali A Torbati, MD................................................................ 584
The Correlation of TIMI Risk Scores with Extent of Coronary Artery Disease in a Multi-Ethnic Patient
Population Presenting with Non-ST Elevation Myocardial Infarction .............................................. 584
NEW YORK POSTER FINALIST - RESEARCH Marius Viseroi, MD ............................................................ 585
Impact of Troponin Elevation Among Critically Ill Patients .............................................................. 585
NORTH CAROLINA POSTER FINALIST - RESEARCH Basem M Mishriky, MD .......................................... 586
The Efficacy and Safety of DPP4 Inhibitors compared to Sulfonylureas as add-on Therapy to
Metformin in Patients with Type 2 diabetes: A Meta-analysis......................................................... 586
NORTH CAROLINA POSTER FINALIST - RESEARCH Rahul Singh, MD ..................................................... 587
"Seven Is the New Ten" – Comprehensive Quality Improvement Project to Adopt Restrictive
Transfusion Strategies in a Community Hospital .............................................................................. 587
A Novel Outpatient Curriculum to Improve Residents’ Awareness and Knowledge of High Value
Care (HVC) ......................................................................................................................................... 589
[Date]
NORTH CAROLINA POSTER FINALIST - RESEARCH Eric Walford, MD .................................................... 589
47
NORTH DAKOTA POSTER FINALIST - RESEARCH Srinivasa Madhavan, MD .......................................... 590
Is There a Gender Disparity in the Management of STEMI?............................................................. 590
OHIO POSTER FINALIST - RESEARCH Shadi M. Al Halabi ....................................................................... 591
Statin Therapy Impact on Postoperative Outcomes in Cardiac Surgery: A Meta-Analysis of
Randomized Controlled Trials ........................................................................................................... 591
OHIO POSTER FINALIST - RESEARCH Yaseen Alastal, MD ..................................................................... 592
The Impact of Fellow Involvement on Quality Measures and Patient Satisfaction of Colonoscopy in
Newly Established Gastroenterology Fellowship Program ............................................................... 592
OHIO POSTER FINALIST - RESEARCH Vyshak Alva Venur, MD............................................................... 594
New disease specific graded prognostic assessment of brain metastasis from lung, breast,
melanoma and renal malignancies. .................................................................................................. 594
OHIO POSTER FINALIST - RESEARCH Maricor Docena, DO ................................................................... 595
Association of Early Physician Follow-up and 30-Day Readmission After Hospitalization for Heart
Failure Among Patients in a Residency-Based Ambulatory Clinic .................................................... 595
OHIO POSTER FINALIST - RESEARCH Tariq Hammad, MD..................................................................... 596
Impact of Rapid On-Site Evaluation with Cytopathologist Guidance on the Diagnostic Yield of EUSFNA of Pancreatic Lesions. ................................................................................................................ 596
OHIO POSTER FINALIST - RESEARCH Bin Hu, MD .................................................................................. 597
Vitamin D Inadequacy in Patients of Northeast Ohio ....................................................................... 597
OHIO POSTER FINALIST - RESEARCH Maksim Y Khayznikov, MD .......................................................... 598
Reversibility of Statin Induced Myalgia and Myositis with High Dose Vitamin D Supplementation.598
OHIO POSTER FINALIST - RESEARCH Aahd Kubbara, MBBS .................................................................. 599
Application of CDC Ventilator-associated Events Surveillance Guidelines for Neurosurgery Patients:
Is it Valid? .......................................................................................................................................... 599
Diagnostic ramifications of ocular vascular occlusion as a first thrombotic event associated with
Factor V Leiden and Prothrombin Gene heterozygosity................................................................... 600
[Date]
OHIO POSTER FINALIST - RESEARCH Samantha L Schockman, MD ...................................................... 600
48
ONTARIO POSTER FINALIST - RESEARCH Elvira R Bangert, MD ............................................................ 601
Non-invasive risk stratification with stress single photon emission computed tomography in
patients with myocardial injury following non-cardiac surgery ....................................................... 601
ONTARIO POSTER FINALIST - RESEARCH Nihal Haque, MD .................................................................. 602
Incidence and Outcomes of Post-Operative Atrial Fibrillation and Supraventricular Arrhythmias: A
Systematic Review and Meta Analysis .............................................................................................. 602
OREGON POSTER FINALIST - RESEARCH Katelyn Atkins, PhD ............................................................... 603
The impact of anatomic tumor location on inter-fraction tumor motion during lung stereotactic
body radiation therapy (SBRT) .......................................................................................................... 603
OREGON POSTER FINALIST - RESEARCH Gita Dorothy Gelfer, DO ........................................................ 604
Impact of Rapid Diagnosis for Community Acquired Pneumonia..................................................... 604
OREGON POSTER FINALIST - RESEARCH Allison C Huang, DO .............................................................. 605
Code Stroke: Shortening Needle Time For Inpatient Brain Attack ................................................... 605
PENNSYLVANIA POSTER FINALIST - RESEARCH Mahmoud S Abdelghany, MD .................................... 606
Reducing severe hypoglycemic events in hospitalized patients with diabetes mellitus: a
multidisciplinary approach................................................................................................................ 606
PENNSYLVANIA POSTER FINALIST - RESEARCH Abhishek Agarwal, MD ............................................... 607
Evaluation of Mentors by Resident and Fellows in a Structured Mentoring Program in an academic
medical center .................................................................................................................................. 607
PENNSYLVANIA POSTER FINALIST - RESEARCH Wuqiang Fan, MD ....................................................... 608
CYP2C19 GENETIC VARIATION AND INDIVIDUALIZED CLOPIDOGREL PRESCRIPTION IN A
CARDIOLOGY CLINIC – A PROSPECTIVE STUDY ................................................................................. 608
PENNSYLVANIA POSTER FINALIST - RESEARCH Sushil Ghimire, MBBS ................................................. 609
Efficacy and Safety of Apixaban for prevention of venous thromboembolism in patients undergoing
Arthroplasty: Systematic Review and Meta-analysis ........................................................................ 609
The ASIN Index: A Novel Tool to Assess Outpatient "No Show" Risk ............................................... 610
[Date]
PENNSYLVANIA POSTER FINALIST - RESEARCH Kristian D Holmes, MD................................................ 610
49
PENNSYLVANIA POSTER FINALIST - RESEARCH Deepanshu Jain, MD ................................................... 611
Effect of different treatment modalities on Colon adenoma and advanced adenoma among Type II
Diabetes Mellitus patients ................................................................................................................ 611
PENNSYLVANIA POSTER FINALIST - RESEARCH Sukrut Nanavaty, MBBS .............................................. 612
Leveraging EMR-driven, team-based Empanelment to improve patient care continuity and
accountability for population management and health. .................................................................. 612
PENNSYLVANIA POSTER FINALIST - RESEARCH Deepak Kumar Pasupula, MD ..................................... 613
Is Left Bundle Branch Block Related to the Mechanism of Left Ventricular Dyssynchrony? ............ 613
PENNSYLVANIA POSTER FINALIST - RESEARCH Paragkumar C Patel, MD, MBBS ................................. 614
The Power of Anecdotes- HVCCC versus Defensive Medicine.......................................................... 614
PENNSYLVANIA POSTER FINALIST - RESEARCH Ranjan Pathak, MBBS ................................................. 615
National Trends in the Use of Mechanical Thrombectomy for Reperfusion Therapy in Acute
Ischemic Stroke ................................................................................................................................. 615
PENNSYLVANIA POSTER FINALIST - RESEARCH Devalkumar J Rajyaguru, MD ..................................... 616
Evaluation of Factors That Impact Hospital Readmission Rates in a Teaching University- Based
Internal Medicine Resident Clinic. .................................................................................................... 616
PENNSYLVANIA POSTER FINALIST - RESEARCH Shelini R Sooklal, MBBS .............................................. 617
Barriers to Colorectal Cancer Screening Colonoscopy in a Suburban Low Income Pennsylvania Clinic.
.......................................................................................................................................................... 617
PENNSYLVANIA POSTER FINALIST - RESEARCH Yin Wu, MD ................................................................. 618
PHARMACOGENETICS-GUIDED INDIVIDUAL WARFARIN DOSING – A PROSPECTIVE OBSERVATORY
STUDY ................................................................................................................................................ 618
RHODE ISLAND POSTER FINALIST - RESEARCH Megha Garg ................................................................. 619
Physician Advocacy: What Do Housestaff Know (and Care) About? ................................................ 619
Cerebral Hyperperfusion Syndrome after Intravenous Thrombolysis for Acute Ischemic Stroke ... 620
[Date]
SINGAPORE - POSTER FINALIST - RESEARCH Mayank Dalakoti, MBBS ................................................. 620
50
SOUTH CAROLINA POSTER FINALIST - RESEARCH Gabriel D McCoy, DO .............................................. 621
A Novel Evaluation of the Positive Predictive Value of the Platelet Factor 4 ELISA in Bacteremia. . 621
TEXAS POSTER FINALIST - RESEARCH Kazeen Nuri Abdullah, MD ........................................................ 622
Resident Engagement in Patient Safety ............................................................................................ 622
TEXAS POSTER FINALIST - RESEARCH Joyce Alencherril, DO ................................................................ 623
Reducing Congestive Heart Failure Readmissions: Success through Collaboration at Methodist
Dallas Medical Center. ...................................................................................................................... 623
TEXAS POSTER FINALIST - RESEARCH Alexander L Bullen Clarke, MD .................................................. 624
Resident-driven quality improvement project to reduce diagnostic errors by the application of
debiasing strategies .......................................................................................................................... 624
TEXAS POSTER FINALIST - RESEARCH Anam Hameed, MD ................................................................... 626
Gastric Electrical Stimulator and its Impact on Symptom Reduction among Gastroparesis Patients
with Prior Cholecystectomy .............................................................................................................. 626
TEXAS POSTER FINALIST - RESEARCH Rajeev Singh, MD....................................................................... 627
Reduction of Time to Treatment, Emergency Department Dwell times, and Cost of Treatment for
Acutely Decompensated Heart Failure using Observation Units and Six Sigma Methodology ........ 627
TEXAS POSTER FINALIST - RESEARCH Rumit P Thakkar, DO.................................................................. 629
A Multifaceted Approach To Reduce Heart Failure (HF) Readmissions ........................................... 629
TEXAS POSTER FINALIST - RESEARCH Jesus Vera-Aguilera, MD............................................................ 630
Combined parasite derived peptide GK1 and Programmed Death antibody (anti-PD-L1) therapy
increased survival in a melanoma mouse model. ............................................................................. 630
US AIR FORCE POSTER FINALIST - RESEARCH CAPT Cassandra L Craig, MD ......................................... 631
Presence of Vitamin B12 Deficiency and Anti-Gastric Parietal Cell Antibodies in Patients with
Rheumatoid Arthritis ........................................................................................................................ 631
Chapter Winning Abstract................................................................................................................. 632
[Date]
US AIR FORCE POSTER FINALIST - RESEARCH Christin Laufer, MD ....................................................... 632
51
US ARMY POSTER FINALIST - RESEARCH CAPT Victoria S Fernandes, MC USA .................................... 633
KETAMINE BY CONTINUOUS INFUSION FOR SEDATION IN SEPTIC SHOCK....................................... 633
US NAVY POSTER FINALIST - RESEARCH Ian Grasso, MD ...................................................................... 634
Chapter Winning Abstract................................................................................................................. 634
UTAH POSTER FINALIST - RESEARCH Sonja Raaum, MD ....................................................................... 635
U.S. resident physician use of smartphones in clinical care ............................................................. 635
VERMONT POSTER FINALIST - RESEARCH Charita Vadlamudi, MD ...................................................... 636
From Past to Present: Continuity of Care in a Resident Clinic after a 4 + 1 Block Schedule
Implementation ................................................................................................................................ 636
WEST VIRGINIA POSTER FINALIST - RESEARCH Colleen Pettrey, MD ................................................... 638
PULMONARY FUNCTION TESTING IN PATIENTS WITH COPD IN THE CAMC OUTPATIENT CARE
CENTER .............................................................................................................................................. 638
WEST VIRGINIA POSTER FINALIST - RESEARCH Muhammad Shabbir Rawala, MD............................... 639
Left Ventricular Ejection Fraction Assessment: Comparison between Single Photon Emission
Computed Tomography and Echocardiography ............................................................................... 639
WISCONSIN POSTER FINALIST - RESEARCH Wei An, MD ...................................................................... 640
Repeat Lipopolysaccharide Exposure is Sufficient to Impair Viral Induced Pro-atopic CD49d
Expressing Neutrophil Recruitment to the Lung............................................................................... 640
RESIDENT FELLOW PODIUM PRESENTATIONS .......................................................................................... 641
COLORADO PODIUM PRESENTATION - RESEARCH Ryan Daniel Murphy, MD ..................................... 642
IMPLEMENTATION OF A “FOUR C’S” REAL-TIME FEEDBACK TOOL TO ASSESS PATIENT SATISFACTION
AND PROVIDER COMMUNICATION .................................................................................................. 642
ILLINOIS PODIUM PRESENTATION - RESEARCH Abdalla Hassan, MD ................................................... 644
Vascular Closure Device Malfunction: What are we missing? .......................................................... 644
[Date]
MICHIGAN PODIUM PRESENTATION - RESEARCH Daniel E Ezekwudo, MD ......................................... 645
52
Methyl Jasmonate: A plant stress hormone that enhances radio-sensitivity of hormone refractory
prostate cancer cells. ........................................................................................................................ 645
MICHIGAN PODIUM PRESENTATION - RESEARCH Suwen Kumar ......................................................... 646
Positive airway pressure affects cardiac remodeling in hypertrophic cardiomyopathy patients with
obstructive sleep apnea .................................................................................................................... 646
NEW JERSEY PODIUM PRESENTATION - RESEARCH Martin Miguel I Amor, MD .................................. 647
IMPROVED EFFICIENCY AND COST SAVINGS FROM TRIAGING SELECTED TRANSIENT ISCHEMIC
ATTACK PATIENTS TO OUTPATIENT URGENT CARE .......................................................................... 647
OHIO PODIUM PRESENTATION - RESEARCH Mahesh Bavineni, MD .................................................... 648
“NOTE BLOAT SYNDROME”: AN EPIDEMIC AFFECTING ELECTRONIC HEALTH RECORDS, HIGH TIME
TO CHANGE SOAP NOTE TO APSO NOTE. ......................................................................................... 648
PENNSYLVANIA PODIUM PRESENTATION - RESEARCH Marvin Louis Roy Lu, MD ............................... 649
Electrocardiographic Changes Consistent with Atrial Infarction are an Independent Predictor of 30
Day and 1 Year Mortality in Patients with Acute ST-Elevation Myocardial Infarction ..................... 649
PENNSYLVANIA PODIUM PRESENTATION - RESEARCH Loheetha Ragupathi, MD ............................... 650
Proton Pump Inhibitors and Hypomagnesemia in Patients with Arrhythmias ................................. 650
QUEBEC PODIUM PRESENTATION - RESEARCH Catherine Matte, MD ................................................. 651
Improving Prescribing Practices on Clinical Teaching Units: Glucocorticoid Use in Chronic
Obstructive Pulmonary Disease Exacerbations ................................................................................ 651
VIRGINIA PODIUM PRESENTATION - RESEARCH John Smirniotopoulos, MD ....................................... 652
In-hospital cost analysis of Prostate Artery Embolization (PAE) and Transurethral Resection of the
Prostate (TURP) in the treatment of Benign Prostatic Hyperplasia. ................................................. 652
RESIDENT FELLOW POSTER FINALISTS ...................................................................................................... 654
ARIZONA POSTER FINALIST - RESEARCH Adebisi Alli, DO ..................................................................... 655
Innovations in Patient Safety Education of Internal Medicine Residents......................................... 655
[Date]
CALIFORNIA POSTER FINALIST - RESEARCH Alan Beneze, MD .............................................................. 656
53
Simplified Pulmonary Embolism Severity Index Accurately Reflects Length of Stay, Readmission and
Death in a California Cohort.............................................................................................................. 656
CALIFORNIA POSTER FINALIST - RESEARCH Seth Blumberg, MD, PhD ................................................. 657
Evaluating the risk of re-emergence of measles in the United States .............................................. 657
CALIFORNIA POSTER FINALIST - RESEARCH Brittany A Doremus, DO................................................... 658
Frequent Premature Atrial Complexes and their Association with Risk of Incident Heart Failure,
Stroke, and All-Cause Mortality. ....................................................................................................... 658
CALIFORNIA POSTER FINALIST - RESEARCH Heather Hofmann, MD .................................................... 660
Teaching on Rounds: Observations, Perceptions, and an Intervention to Increase Bedside Teaching
.......................................................................................................................................................... 660
CALIFORNIA POSTER FINALIST - RESEARCH Jisha K Joshua, MD ........................................................... 661
SOLUBLE GUANYLATE CYCLASE AS A NOVEL TREATMENT TARGET FOR OSTEOPOROSIS ................. 661
CALIFORNIA POSTER FINALIST - RESEARCH Lucy Liu, MD ..................................................................... 662
Racial Ethnic Differences in Hip Fracture Incidence and Mortality in Older Men ............................ 662
CALIFORNIA POSTER FINALIST - RESEARCH Mala C Mandyam, MD ..................................................... 663
Discharge checklists may reduce medical errors. ............................................................................. 663
CALIFORNIA POSTER FINALIST - RESEARCH Sajan Patel, MD ................................................................ 664
Appropriate Utilization of Telemetry ................................................................................................ 664
CALIFORNIA POSTER FINALIST - RESEARCH Ray Pillai, MD ................................................................... 665
Change in Pulse Oximetry Waveform Before and After Hemodialysis and Ultrafiltration in Critically
Ill Patients May Reflect Hemodynamics ........................................................................................... 665
CALIFORNIA POSTER FINALIST - RESEARCH Veronica Ramirez, MD ..................................................... 666
Health in one touch: Assessing the use of mobile health information by patients of LAC+USC
Medical Center Primary Care Clinics ................................................................................................. 666
[Date]
CALIFORNIA POSTER FINALIST - RESEARCH Linnaea Schuttner, MD .................................................... 667
54
The MyCare pilot: Improving non-urgent ED utilization and inpatient admission through ambulatory
multidisciplinary care ........................................................................................................................ 667
CALIFORNIA POSTER FINALIST - RESEARCH Sarthi R Shah, MD ............................................................ 668
Utilization of G Charts to Analyze Rare Occurrence Events in Health Care Quality Improvement .. 668
CALIFORNIA POSTER FINALIST - RESEARCH Viet Tran, DO .................................................................... 669
Percentage of Patients with Gram Positive Bacteremia, Meningitis,Hospital-Acquired Pneumonia,
Severe Sepsis, or Septic Shock who Achieve a Therapeutic First Vancomycin Trough .................... 669
COLORADO POSTER FINALIST - RESEARCH Claudia Ihm, MD ............................................................... 670
Clinical characteristics of patients diagnosed with community-associated Clostridium difficile
infection ............................................................................................................................................ 670
COLORADO POSTER FINALIST - RESEARCH Kara R Mizokami-Stout, MD.............................................. 671
Evaluation of the Appropriate Use and Safety of Intravenous Levothyroxine at an Academic Medical
Center................................................................................................................................................ 671
CONNECTICUT POSTER FINALIST - RESEARCH Theo Borgovan, MD ..................................................... 672
The Role of Cancer Stem Cells in Gauging Follicular Lymphoma Prognosis ..................................... 672
CONNECTICUT POSTER FINALIST - RESEARCH Kofi M Osei, MD ........................................................... 673
The impact of an awareness campaign on hospital cost reduction and redundant laboratory testing
in a community teaching hospital ..................................................................................................... 673
DELAWARE POSTER FINALIST - RESEARCH Nirmol Philip, MD .............................................................. 675
Supersize This - Improving Resident Communication about Obesity in the Outpatient Clinic ........ 675
DELAWARE POSTER FINALIST - RESEARCH Xian Qiao, MD ................................................................... 677
Reflex to Urine Culture: Truncating the Time Taken to Transport the Tinkle to the Testing ........... 677
FLORIDA POSTER FINALIST - RESEARCH Lucas A Burke, MD ................................................................. 678
Positive predictive value of elevated troponin for diagnosis of acute coronary syndrome ............. 678
[Date]
FLORIDA POSTER FINALIST - RESEARCH Maroun Sfeir, MD .................................................................. 679
55
Clinical Laboratory Practices in Speciating Organisms and Reporting Results of Voided Urine
Cultures ............................................................................................................................................. 679
GEORGIA POSTER FINALIST - RESEARCH Salim Hayek, MD .................................................................. 681
College Education is an Independent Predictor of Survival in Patients with Heart Disease or
Cardiovascular Risk Factors Who Undergo Left Heart Catheterization ............................................ 681
GEORGIA POSTER FINALIST - RESEARCH Anthony S Otekeiwebia, MBBS............................................. 682
Performance of Oxygen Saturation Index in Adults with Type 1 Respiratory Failure ...................... 682
GEORGIA POSTER FINALIST - RESEARCH Ayman Samman Tahhan, MD ............................................... 683
Circulating progenitor cells are an independent predictor of coronary artery disease progression 683
HAWAII POSTER FINALIST - RESEARCH Pamela Sebastian, MD, MBBS................................................. 684
Provider Orders for Life-Sustaining Treatment (POLST) Implementation and Training in Nursing
Facilities in Hawaii ............................................................................................................................. 684
ILLINOIS POSTER FINALIST - RESEARCH Pakhadi H Buddhadev, MBBS ................................................. 685
Correlation between Blood Glucose levels and duration of Mechanical Ventilation....................... 685
ILLINOIS POSTER FINALIST - RESEARCH Briana T Costello, MD ............................................................. 686
IF YOUR PATIENT HAS-BLED, DID YOU CALCULATE THE CHA2DS2-VASc SCORE? ............................ 686
ILLINOIS POSTER FINALIST - RESEARCH Manjusha Das, MD ................................................................. 687
Antibiogram of VRE causing Urinary Tract Infections as a retrospective study from MMC, Springfield
Illinois ................................................................................................................................................ 687
ILLINOIS POSTER FINALIST - RESEARCH Lindsay M Esch, MD ............................................................... 688
Preparing for the Primary Care Clinic: An Ambulatory Boot Camp for Internal Medicine Interns... 688
ILLINOIS POSTER FINALIST - RESEARCH Adriana G Olariu, MD ............................................................. 689
Risk of Crohn’s Disease Recurrence after Surgical Resection: Implications of Tobacco Use and
Preoperative Corticosteroids ............................................................................................................ 689
[Date]
ILLINOIS POSTER FINALIST - RESEARCH Karthik Ragunathan, MD ........................................................ 690
56
Rates of infection for single vs multilumen peripherally inserted central catheter: A systematic
review................................................................................................................................................ 690
INDIANA POSTER FINALIST - RESEARCH Emily Cochard, MD ................................................................ 692
Impact of Evidence-Based Guidelines for Management of Clostridium Difficile Infection .............. 692
INDIANA POSTER FINALIST - RESEARCH Stephanie N Martin, MD ....................................................... 693
Evaluation of discrepancies in statin use recommendations between ATP3 and ACC/AHA lipid
guidelines in a primary care population ........................................................................................... 693
INDIANA POSTER FINALIST - RESEARCH Stephen Schutzman, MD ....................................................... 694
The Cost of A Cardiac Marker:It’s Enough to Give You Chest Pain ................................................... 694
IOWA POSTER FINALIST - RESEARCH Chad C Ward, MD ....................................................................... 695
DETECTION OF ARRHYTHMIC EVENTS: AN ASSESSMENT OF SCREENING ........................................ 695
KANSAS POSTER FINALIST - RESEARCH Allison J Baughman, MD ......................................................... 696
Effects of Revised Consultation Room Design on Patient-Physician Communication ...................... 696
KANSAS POSTER FINALIST - RESEARCH Kaitlin M Ditch, MD ................................................................ 697
Barriers to Enter Weight Maintenance ............................................................................................. 697
KANSAS POSTER FINALIST - RESEARCH Youness Hussein, MD ............................................................. 698
IMPROVING ANTICOAGULATION MANAGEMENT ............................................................................ 698
KANSAS POSTER FINALIST - RESEARCH Mohinder Reddy Vindhyal, MD .............................................. 700
Cardio-Renal association for heart failure re-admissions ................................................................. 700
KENTUCKY POSTER FINALIST - RESEARCH Anub G John, MD................................................................ 701
Changes in Glomerular Filtration Rate (GFR) following implantation of Continuous Flow Left
Ventricular Assist Devices (LVAD) ..................................................................................................... 701
Does the addition of adjuvant intraoperative post-dissection tumor bed chemotherapy during GI
neuroendocrine tumor debulking benefit patients? ........................................................................ 703
[Date]
LOUISIANA POSTER FINALIST - RESEARCH Aman Chauhan, MBBS ....................................................... 703
57
MARYLAND POSTER FINALIST - RESEARCH Paul E Miller II, MD ........................................................... 704
HIV and Coronary Arterial Remodeling from the Multicenter AIDS Cohort Study (MACS) .............. 704
MASSACHUSETTS POSTER FINALIST - RESEARCH Fadi Alkhatib, DO..................................................... 705
Long Eye Lashes, and Too long To See Them! .................................................................................. 705
MASSACHUSETTS POSTER FINALIST - RESEARCH Theodora Anagnostou, MD ..................................... 706
The effects of Candida Colonization and antifungal use on the outcomes of patients with VentilatorAssociated Pneumonia ...................................................................................................................... 706
MASSACHUSETTS POSTER FINALIST - RESEARCH Hari Pokharel, MD ................................................... 707
The Baystate Frailty Study – Prevalence of Frailty in a Cohort of Hospitalized Elderly Patients ...... 707
MASSACHUSETTS POSTER FINALIST - RESEARCH Zirui Song, MD ......................................................... 708
Changes in Health Care Spending and Quality 4 Years into Global Payment for Accountable Care
Organizations .................................................................................................................................... 708
MEXICO - POSTER FINALIST - RESEARCH Sonia Rodriguez, MD ............................................................ 709
Prevalence of pathology renal findings not associated to disease activity in patients with Systemic
Lupus Erythematosus (SLE). .............................................................................................................. 709
MEXICO - POSTER FINALIST - RESEARCH Jorge Rafael Romo Tena, MD ............................................... 710
The E3 ligase Casitas B Lineage Lymphoma b (Cbl-b) Modulates Peripheral Regulatory T cell
Function via p27kip1 in patients with Systemic Lupus Erythematosus. ........................................... 710
MICHIGAN POSTER FINALIST - RESEARCH Sourabh Aggarwal, MBBS................................................... 711
Epidemiology of Takotsubo cardiomyopathy in US: An analysis of NIS data ................................... 711
MICHIGAN POSTER FINALIST - RESEARCH Daniel E Ezekwudo, MD ..................................................... 712
Chapter Winning Abstract................................................................................................................. 712
MICHIGAN POSTER FINALIST - RESEARCH Timothy A Joseph, MD ....................................................... 713
MICHIGAN POSTER FINALIST - RESEARCH Devin Birsingh Malik, MD ................................................... 714
[Date]
Cost of Mediterranean Diet Compared to Dietary Expenditures Recommended by the United States
Department of Agriculture................................................................................................................ 713
58
How did the United States Preventative Services Task Force 2005 Guidelines for Abdominal Aortic
Aneurysm Screening Affect Mortality in the United States Population? ......................................... 714
MINNESOTA POSTER FINALIST - RESEARCH Vidhu Anand, MBBS ........................................................ 715
Ofatumumab for Rheumatoid Arthritis: A Cochrane Systematic Review and Meta-analysis .......... 715
MINNESOTA POSTER FINALIST - RESEARCH Joel D Beachey, MD ......................................................... 717
Reducing Unnecessary Routine Lab Tests for Hospitalized Medical Patients .................................. 717
MINNESOTA POSTER FINALIST - RESEARCH Thoetchai Peeraphatdit, MD ........................................... 718
The Relationship between Serum Electrolytes and Electrocardiographic Intervals ......................... 718
MINNESOTA POSTER FINALIST - RESEARCH Paolo Strati, MD .............................................................. 719
Renal Complications of Chronic Lymphocytic Leukemia/Monoclonal B-cell Lymphocytosis (CLL/MBL)
.......................................................................................................................................................... 719
MINNESOTA POSTER FINALIST - RESEARCH Priya Vijayvargiya, MD..................................................... 720
Characterization of hypothalamic hunger and satiety signals with pulsed arterial spin labeling MRI
.......................................................................................................................................................... 720
MISSISSIPPI POSTER FINALIST - RESEARCH Ben Horton, MD ................................................................ 722
Analysis of a Guideline-Derived Resident Educational Program on Inpatient Glycemic Control ..... 722
MISSISSIPPI POSTER FINALIST - RESEARCH Arnaldo F Lopez-Ruiz, MD................................................. 723
Protective Role of Acute Testosterone Infusion during Acute Kidney Injury (AKI)........................... 723
MISSOURI POSTER FINALIST - RESEARCH Purvi G Patel, MD ................................................................ 724
Incorporation of the 2013 ACC/AHA Lipid Guidelines into the Management of Patients with
Diabetes ............................................................................................................................................ 724
MISSOURI POSTER FINALIST - RESEARCH Dhivya Sugumar, MBBS ....................................................... 726
Improving documentation of Advance Directives and Code status in the outpatient setting by
Resident Physicians ........................................................................................................................... 726
[Date]
MISSOURI POSTER FINALIST - RESEARCH Li Zhou, MD ......................................................................... 727
59
Extracorporeal photopheresis as second-line treatment for acute graft-versus-host disease: Impact
on six month freedom from treatment failure ................................................................................. 727
NEVADA POSTER FINALIST - RESEARCH Amhoud Farooq, MBBS ......................................................... 728
Unexpected effects of amino acids and NMDA receptor in the treatment of Acute liver failure and
acetaminophen hepatotoxicity. ........................................................................................................ 728
NEVADA POSTER FINALIST - RESEARCH Shahrukh Hussain Khan, MBBS .............................................. 729
Practices and Utilization of DVT Prophylaxis at a Community Hospital ........................................... 729
NEW JERSEY POSTER FINALIST - RESEARCH Abhinav Agrawal, MD ...................................................... 730
Are we being an Oxy-moron : The overuse of oxygen in a community hospital setting. ................. 730
NEW JERSEY POSTER FINALIST - RESEARCH Abhinav Agrawal, MD ...................................................... 731
Monmouth Emergency Evaluation Tool ( MEET) - a unique tool to predict observation status. ..... 731
NEW JERSEY POSTER FINALIST - RESEARCH Tasnim Imran, MD ........................................................... 732
Association of Obstructive Sleep Apnea and Pulmonary Hypertension: a meta-analysis ................ 732
NEW JERSEY POSTER FINALIST - RESEARCH Nara Lee, MD ................................................................... 733
Peritoneal Carcinomatosis in Colorectal Cancer: Proposed Algorithm for Cytoreduction/HIPEC .... 733
NEW JERSEY POSTER FINALIST - RESEARCH Abdul Hameed Zaid, MBBS .............................................. 734
Interprofessional education: establishing a collaborative medicine-pharmacy research program. 734
NEW MEXICO POSTER FINALIST - RESEARCH Christopher Bunn, DO ................................................... 736
Improving the Documentation of Nutritional Supplements in an Outpatient Primary Care Clinic .. 736
NEW MEXICO POSTER FINALIST - RESEARCH Benjamin R Deaton, MD ............................................... 737
Trajectory and Long Term Outcomes in Patients with MRSA bacteremia ....................................... 737
NEW YORK POSTER FINALIST - RESEARCH Puvanalingam Ayyadurai, MBBS ........................................ 738
[Date]
HIV ASSOCIATED PULMONARY ARTERIAL HYPERTENSION IN A COHORT OF HIV INFECTED AFRICAN
AMERICANS. ...................................................................................................................................... 738
60
NEW YORK POSTER FINALIST - RESEARCH Amit Bhanvadia, MD .......................................................... 739
Shifts in the Microbiota Following Antibiotic Therapy for Clostridium difficile Infection Favor
Enterobacteriaceae ........................................................................................................................... 739
NEW YORK POSTER FINALIST - RESEARCH Sunny Goel, MD ................................................................. 740
Relationship of Body Mass Index With All-Cause and Cardiovascular Mortality and Hospitalizations
in Patients with Chronic Heart Failure- "The Obesity Paradox" ....................................................... 740
NEW YORK POSTER FINALIST - RESEARCH Huijuan Liao, MD ............................................................... 741
The Etiology and Risk Factor Analysis in Hypercalcemic Crisis ......................................................... 741
NEW YORK POSTER FINALIST - RESEARCH Ronald A Luna, MD ............................................................ 742
Patient satisfaction: Is it linked to quality and cost of care? ............................................................ 742
NEW YORK POSTER FINALIST - RESEARCH Naoki Misumida, MD ......................................................... 743
Absence of ST Elevation in Lead V1 Predicts Worse Long-term Outcomes in Patients with First
Anterior ST Elevation Myocardial Infarction ..................................................................................... 743
NEW YORK POSTER FINALIST - RESEARCH Amer Nazir, MD, MBBS ...................................................... 744
Indwelling Urinary Catheters in Hospitalized Patients: Appropriate Use, Discontinuation and Followup: A Quality Improvement (QI) Project ........................................................................................... 744
NEW YORK POSTER FINALIST - RESEARCH Alejandro Recio Boiles, MD ............................................... 745
Evaluation of a Practical Low-Cost Quality Intervention to Improve Adherence to Evidence-Based
Cancer Screening Recommendations in 642 Patients ...................................................................... 745
NEW YORK POSTER FINALIST - RESEARCH Daniel C Rodriguez, MD ..................................................... 746
Is echocardiogram and left ventriculography both necessary in patients undergoing elective left
heart catheterization? ...................................................................................................................... 746
NEW YORK POSTER FINALIST - RESEARCH Naveen Sablani, MD........................................................... 747
Does an Upright T Wave in Lead V1 Predict Left Anterior Descending Artery Lesion and/or a Left
Circumflex Artery Lesion on Cardiac Catheterization? ..................................................................... 747
[Date]
NEW YORK POSTER FINALIST - RESEARCH Anawin Sanguankeo, MD ................................................... 748
61
Association Between NSAIDs and Clostridium difficile-associated Diarrhea (CDAD): a Systematic
Review and Meta-Analysis ................................................................................................................ 748
NEW YORK POSTER FINALIST - RESEARCH Ali A Torbati, MD................................................................ 749
The Correlation of TIMI Risk Scores with Extent of Coronary Artery Disease in a Multi-Ethnic Patient
Population Presenting with Non-ST Elevation Myocardial Infarction .............................................. 749
NEW YORK POSTER FINALIST - RESEARCH Marius Viseroi, MD ............................................................ 750
Impact of Troponin Elevation Among Critically Ill Patients .............................................................. 750
NORTH CAROLINA POSTER FINALIST - RESEARCH Basem M Mishriky, MD .......................................... 751
The Efficacy and Safety of DPP4 Inhibitors compared to Sulfonylureas as add-on Therapy to
Metformin in Patients with Type 2 diabetes: A Meta-analysis......................................................... 751
NORTH CAROLINA POSTER FINALIST - RESEARCH Rahul Singh, MD ..................................................... 752
"Seven Is the New Ten" – Comprehensive Quality Improvement Project to Adopt Restrictive
Transfusion Strategies in a Community Hospital .............................................................................. 752
NORTH CAROLINA POSTER FINALIST - RESEARCH Eric Walford, MD .................................................... 754
A Novel Outpatient Curriculum to Improve Residents’ Awareness and Knowledge of High Value
Care (HVC) ......................................................................................................................................... 754
NORTH DAKOTA POSTER FINALIST - RESEARCH Srinivasa Madhavan, MD .......................................... 755
Is There a Gender Disparity in the Management of STEMI?............................................................. 755
OHIO POSTER FINALIST - RESEARCH Shadi M. Al Halabi ....................................................................... 756
Statin Therapy Impact on Postoperative Outcomes in Cardiac Surgery: A Meta-Analysis of
Randomized Controlled Trials ........................................................................................................... 756
OHIO POSTER FINALIST - RESEARCH Yaseen Alastal, MD ..................................................................... 757
The Impact of Fellow Involvement on Quality Measures and Patient Satisfaction of Colonoscopy in
Newly Established Gastroenterology Fellowship Program ............................................................... 757
New disease specific graded prognostic assessment of brain metastasis from lung, breast,
melanoma and renal malignancies. .................................................................................................. 759
[Date]
OHIO POSTER FINALIST - RESEARCH Vyshak Alva Venur, MD............................................................... 759
62
OHIO POSTER FINALIST - RESEARCH Maricor Docena, DO ................................................................... 760
Association of Early Physician Follow-up and 30-Day Readmission After Hospitalization for Heart
Failure Among Patients in a Residency-Based Ambulatory Clinic .................................................... 760
OHIO POSTER FINALIST - RESEARCH Tariq Hammad, MD..................................................................... 761
Impact of Rapid On-Site Evaluation with Cytopathologist Guidance on the Diagnostic Yield of EUSFNA of Pancreatic Lesions. ................................................................................................................ 761
OHIO POSTER FINALIST - RESEARCH Bin Hu, MD .................................................................................. 762
Vitamin D Inadequacy in Patients of Northeast Ohio ....................................................................... 762
OHIO POSTER FINALIST - RESEARCH Maksim Y Khayznikov, MD .......................................................... 763
Reversibility of Statin Induced Myalgia and Myositis with High Dose Vitamin D Supplementation.763
OHIO POSTER FINALIST - RESEARCH Aahd Kubbara, MBBS .................................................................. 764
Application of CDC Ventilator-associated Events Surveillance Guidelines for Neurosurgery Patients:
Is it Valid? .......................................................................................................................................... 764
OHIO POSTER FINALIST - RESEARCH Samantha L Schockman, MD ...................................................... 765
Diagnostic ramifications of ocular vascular occlusion as a first thrombotic event associated with
Factor V Leiden and Prothrombin Gene heterozygosity................................................................... 765
ONTARIO POSTER FINALIST - RESEARCH Elvira R Bangert, MD ............................................................ 766
Non-invasive risk stratification with stress single photon emission computed tomography in
patients with myocardial injury following non-cardiac surgery ....................................................... 766
ONTARIO POSTER FINALIST - RESEARCH Nihal Haque, MD .................................................................. 767
Incidence and Outcomes of Post-Operative Atrial Fibrillation and Supraventricular Arrhythmias: A
Systematic Review and Meta Analysis .............................................................................................. 767
OREGON POSTER FINALIST - RESEARCH Katelyn Atkins, PhD ............................................................... 768
The impact of anatomic tumor location on inter-fraction tumor motion during lung stereotactic
body radiation therapy (SBRT) .......................................................................................................... 768
Impact of Rapid Diagnosis for Community Acquired Pneumonia..................................................... 769
[Date]
OREGON POSTER FINALIST - RESEARCH Gita Dorothy Gelfer, DO ........................................................ 769
63
OREGON POSTER FINALIST - RESEARCH Allison C Huang, DO .............................................................. 770
Code Stroke: Shortening Needle Time For Inpatient Brain Attack ................................................... 770
PENNSYLVANIA POSTER FINALIST - RESEARCH Mahmoud S Abdelghany, MD .................................... 771
Reducing severe hypoglycemic events in hospitalized patients with diabetes mellitus: a
multidisciplinary approach................................................................................................................ 771
PENNSYLVANIA POSTER FINALIST - RESEARCH Abhishek Agarwal, MD ............................................... 772
Evaluation of Mentors by Resident and Fellows in a Structured Mentoring Program in an academic
medical center .................................................................................................................................. 772
PENNSYLVANIA POSTER FINALIST - RESEARCH Wuqiang Fan, MD ....................................................... 773
CYP2C19 GENETIC VARIATION AND INDIVIDUALIZED CLOPIDOGREL PRESCRIPTION IN A
CARDIOLOGY CLINIC – A PROSPECTIVE STUDY ................................................................................. 773
PENNSYLVANIA POSTER FINALIST - RESEARCH Sushil Ghimire, MBBS ................................................. 774
Efficacy and Safety of Apixaban for prevention of venous thromboembolism in patients undergoing
Arthroplasty: Systematic Review and Meta-analysis ........................................................................ 774
PENNSYLVANIA POSTER FINALIST - RESEARCH Kristian D Holmes, MD................................................ 775
The ASIN Index: A Novel Tool to Assess Outpatient "No Show" Risk ............................................... 775
PENNSYLVANIA POSTER FINALIST - RESEARCH Deepanshu Jain, MD ................................................... 776
Effect of different treatment modalities on Colon adenoma and advanced adenoma among Type II
Diabetes Mellitus patients ................................................................................................................ 776
PENNSYLVANIA POSTER FINALIST - RESEARCH Sukrut Nanavaty, MBBS .............................................. 777
Leveraging EMR-driven, team-based Empanelment to improve patient care continuity and
accountability for population management and health. .................................................................. 777
PENNSYLVANIA POSTER FINALIST - RESEARCH Deepak Kumar Pasupula, MD ..................................... 778
Is Left Bundle Branch Block Related to the Mechanism of Left Ventricular Dyssynchrony? ............ 778
The Power of Anecdotes- HVCCC versus Defensive Medicine.......................................................... 779
[Date]
PENNSYLVANIA POSTER FINALIST - RESEARCH Paragkumar C Patel, MD, MBBS ................................. 779
64
PENNSYLVANIA POSTER FINALIST - RESEARCH Ranjan Pathak, MBBS ................................................. 780
National Trends in the Use of Mechanical Thrombectomy for Reperfusion Therapy in Acute
Ischemic Stroke ................................................................................................................................. 780
PENNSYLVANIA POSTER FINALIST - RESEARCH Devalkumar J Rajyaguru, MD ..................................... 781
Evaluation of Factors That Impact Hospital Readmission Rates in a Teaching University- Based
Internal Medicine Resident Clinic. .................................................................................................... 781
PENNSYLVANIA POSTER FINALIST - RESEARCH Shelini R Sooklal, MBBS .............................................. 782
Barriers to Colorectal Cancer Screening Colonoscopy in a Suburban Low Income Pennsylvania Clinic.
.......................................................................................................................................................... 782
PENNSYLVANIA POSTER FINALIST - RESEARCH Yin Wu, MD ................................................................. 783
PHARMACOGENETICS-GUIDED INDIVIDUAL WARFARIN DOSING – A PROSPECTIVE OBSERVATORY
STUDY ................................................................................................................................................ 783
RHODE ISLAND POSTER FINALIST - RESEARCH Megha Garg ................................................................. 784
Physician Advocacy: What Do Housestaff Know (and Care) About? ................................................ 784
SINGAPORE - POSTER FINALIST - RESEARCH Mayank Dalakoti, MBBS ................................................. 785
Cerebral Hyperperfusion Syndrome after Intravenous Thrombolysis for Acute Ischemic Stroke ... 785
SOUTH CAROLINA POSTER FINALIST - RESEARCH Gabriel D McCoy, DO .............................................. 786
A Novel Evaluation of the Positive Predictive Value of the Platelet Factor 4 ELISA in Bacteremia. . 786
TEXAS POSTER FINALIST - RESEARCH Kazeen Nuri Abdullah, MD ........................................................ 787
Resident Engagement in Patient Safety ............................................................................................ 787
TEXAS POSTER FINALIST - RESEARCH Joyce Alencherril, DO ................................................................ 788
Reducing Congestive Heart Failure Readmissions: Success through Collaboration at Methodist
Dallas Medical Center. ...................................................................................................................... 788
Resident-driven quality improvement project to reduce diagnostic errors by the application of
debiasing strategies .......................................................................................................................... 789
[Date]
TEXAS POSTER FINALIST - RESEARCH Alexander L Bullen Clarke, MD .................................................. 789
65
TEXAS POSTER FINALIST - RESEARCH Anam Hameed, MD ................................................................... 791
Gastric Electrical Stimulator and its Impact on Symptom Reduction among Gastroparesis Patients
with Prior Cholecystectomy .............................................................................................................. 791
TEXAS POSTER FINALIST - RESEARCH Rajeev Singh, MD....................................................................... 792
Reduction of Time to Treatment, Emergency Department Dwell times, and Cost of Treatment for
Acutely Decompensated Heart Failure using Observation Units and Six Sigma Methodology ........ 792
TEXAS POSTER FINALIST - RESEARCH Rumit P Thakkar, DO.................................................................. 794
A Multifaceted Approach To Reduce Heart Failure (HF) Readmissions ........................................... 794
TEXAS POSTER FINALIST - RESEARCH Jesus Vera-Aguilera, MD............................................................ 795
Combined parasite derived peptide GK1 and Programmed Death antibody (anti-PD-L1) therapy
increased survival in a melanoma mouse model. ............................................................................. 795
US AIR FORCE POSTER FINALIST - RESEARCH CAPT Cassandra L Craig, MD ......................................... 796
Presence of Vitamin B12 Deficiency and Anti-Gastric Parietal Cell Antibodies in Patients with
Rheumatoid Arthritis ........................................................................................................................ 796
US AIR FORCE POSTER FINALIST - RESEARCH Christin Laufer, MD ....................................................... 797
Chapter Winning Abstract................................................................................................................. 797
US ARMY POSTER FINALIST - RESEARCH CAPT Victoria S Fernandes, MC USA .................................... 798
KETAMINE BY CONTINUOUS INFUSION FOR SEDATION IN SEPTIC SHOCK....................................... 798
US NAVY POSTER FINALIST - RESEARCH Ian Grasso, MD ...................................................................... 799
Chapter Winning Abstract................................................................................................................. 799
UTAH POSTER FINALIST - RESEARCH Sonja Raaum, MD ....................................................................... 800
U.S. resident physician use of smartphones in clinical care ............................................................. 800
VERMONT POSTER FINALIST - RESEARCH Charita Vadlamudi, MD ...................................................... 801
WEST VIRGINIA POSTER FINALIST - RESEARCH Colleen Pettrey, MD ................................................... 803
[Date]
From Past to Present: Continuity of Care in a Resident Clinic after a 4 + 1 Block Schedule
Implementation ................................................................................................................................ 801
66
PULMONARY FUNCTION TESTING IN PATIENTS WITH COPD IN THE CAMC OUTPATIENT CARE
CENTER .............................................................................................................................................. 803
WEST VIRGINIA POSTER FINALIST - RESEARCH Muhammad Shabbir Rawala, MD............................... 804
Left Ventricular Ejection Fraction Assessment: Comparison between Single Photon Emission
Computed Tomography and Echocardiography ............................................................................... 804
WISCONSIN POSTER FINALIST - RESEARCH Wei An, MD ...................................................................... 805
[Date]
Repeat Lipopolysaccharide Exposure is Sufficient to Impair Viral Induced Pro-atopic CD49d
Expressing Neutrophil Recruitment to the Lung............................................................................... 805
67
[Date]
RESIDENT FELLOW VIGNETTE PODIUM PRESENTATIONS
68
ARIZONA PODIUM PRESENTATION - CLINICAL VIGNETTE Irbaz Riaz, MD
Loperamide Induced Cardiac Dysrhythmias – An Emerging Toxicological
Phenomenon
First Author: Irbaz Bin Riaz, MD MM, Evbu Enakpene, M.D., Mazda Shirazi M.D. Yuval Raz, M.D. Julia H.
Indik, MD, PhD
Introduction: Loperamide (poor man’s methadone) is an easily available over-the-counter anti-diaarhea
drug. We present a case of 25-year-old female with recurrent hospitalizations secondary to unidentified
loperamide cardio-toxicity.
Case Presentation: A 25-year-old female with no known medical problems initially presented with
abdominal discomfort for 2 weeks. Routine work up for abdominal pain was unrevealing and she was
discharged with pantoprazole script. She was re-admitted 2 weeks later after a syncopal episode. Based
on history and cardiac work-up, she was diagnosed with long QT syndrome and a dual chamber ICD was
implanted. After 6 weeks of ICD placement, she again presented with nausea, vomiting, bradycardia and
hypotensive shock. Initial blood work showed arterial pH of 7.2, hyperkalemia (K: 6 meq/L) , BUN
29mg/dl, creatinine 2.8 mg/dl, and magnesium of 2 mg/dl. Despite correction of potassium and
administration of atropine, she remained bradycardic. Transcutaneous pacing failed to capture. ICD
Interrogation revealed markedly elevated pacing thresholds and normal lead position was confirmed on
chest X-ray. She was intubated for airway protection and required multiple pressors due to
hemodynamic instability. Serial electrocardiograms revealed persistently widened and bizarre paced
QRS complexes. She also had multiple episodes of polymorphic ventricular tachycardia. Drug toxicity
was suspected due to markedly widened paced QRS complex. Initial toxicological screening was
negative. Detailed questioning of her partner then revealed that there were empty bottles of
loperamide in her apartment. Subsequent testing then confirmed the presence of loperamide
metabolites. She recovered completely with Intralipid and supportive therapy in the intensive care unit.
She admitted to chronic abuse of loperamide as a substitute to opioids. She was re-admitted 2 months
later in cardiogenic shock after resuming loperamide abuse and died 18 hours after admission despite
placement on Extracorporeal Membrane Oxygenation (ECMO).
[Date]
Discussion: This case illustrates that loperamide can cause life-threatening heart rhythm disturbances
which can be difficult to diagnose, as the presentation is not unique, can mimic other arrhythmia
disorders such as long QT syndrome and history is often unavailable or unreliable. Thorough
toxicological evaluation should be strongly considered before pacemaker placement in young and
otherwise healthy patients with syncope and an abnormal baseline ECG. Loperamide should be clearly
recognized and labelled as a drug of abuse because it is known to be taken in massive dosages to
substitute for opioids. Currently, it is easily available in large quantities over the counter without any
government regulation. The combination of easy availability at low cost, unregulated websites
increasing awareness about the abuse, lack of awareness about potential fatal rhythm disturbances,
both by patients and physician and complex management requiring multidisciplinary teams deserves
immediate attention of drug regulation authorities and physicians to prevent similar fatal events.
69
MARYLAND PODIUM PRESENTATION - CLINICAL VIGNETTE Candice Crichlow, MD
Hypertensive Encephalopathy or more? Posterior Reversible Encephalopathy
Syndrome and a novel treatment.
First Author: Candice Crichlow, MD Co-Author: Gabriela Molina, MD
Hypertensive emergency is elevated blood pressure resulting in acute end-organ damage which can
include hypertensive encephalopathy. Modern day advances in radiology have established a new
syndrome called Posterior Reversible Encephalopathy Syndrome (PRES). Although this clinicoradiological
diagnosis is not always associated with hypertension, the neurological and radiographical changes are
potentially reversible. Without withdrawing the inciting factors however, irreversible neurological
damage can occur. This case describes one man who presented with a headache and received a novel
treatment for PRES.
A 40 year old African American male with a history of hypertension, non-compliant with medications,
presented to the emergency department with a three day history of headache, malaise, generalized
body aches, nausea, vomiting and blurry vision. His vital signs revealed a blood pressure of 264/169 but
otherwise within normal limits. His neurological exam showed no papilledema, no nystagmus, normal
motor, sensory systems, negative Babinski signs bilaterally and although lethargic, he was completely
oriented to all spheres. The rest of his physical exam was benign.
A CT scan of his head done in the emergency room showed confluent hypodensity of bilateral cerebellar
hemispheres with edema and compression of the fourth ventricle. There was marked enlargement of
the third and fourth ventricles compared to previous imaging, which is consistent with hydrocephalus.
The appearance raised suspicion for PRES.
Given the severity of the changes, the patient‘s blood pressure was controlled with Nicardipine and as
suggested by the consulting neurologist, Mannitol was given to decrease the edema. Seven hours later
on the day of admission, his blood pressure was 170/ 110 and an MRI was performed which showed
resolution of the hydrocephalus and edema. His headache was improved.
[Date]
PRES is characterized by altered mentation in the form of loss of orientation, headaches, decreased level
of consciousness, nausea, visual disturbances and even focal neurological signs along with
radiographical evidence of cerebral imaging abnormalities predominantly in the posterior white matter.
The causes are vast, including cytotoxic agents, hypertension, sepsis, autoimmune diseases and preeclampsia. The pathophysiology is controversial but vasogenic edema is the end result regardless of the
mechanism. Treatment is the removal of the offending agent or treatment of the underlying condition.
In this case, mannitol was used since there was evidence of increased intracranial pressure. Mannitol
has been compared to Magnesium Sulfate for the treatment of PRES in eclampsia but its use was never
described in the setting of hypertensive emergency. This case of quick reversal of radiographic findings
is an indication that mannitol may be used to augment the treatment of PRES.
70
MASSACHUSETTS PODIUM PRESENTATION - CLINICAL VIGNETTE Fadi Alkhatib, DO
Too little can make you bleed, too much can give you a heart attack!
First Author: Fadi Alkhatib, DO Second Author: Sami Ibrahimi MD Third Author: Khawar Maqsood MD
CASE: A 42-year-old female with systemic lupus erythematosus, immune thrombocytopenic purpura
(ITP) and refractory thrombocytopenia requiring splenectomy, presented with persistent substernal
chest pain and found to have new left bundle branch block on electrocardiogram. She had normal vital
signs. She takes Eltrombopag, a thrombopoitin agonist, for ITP and her platelet counts have been known
to fluctuate between 1k/mm3 and more than 1500k/mm3 within the preceding 1 year. Her past medical
history was also significant for a recent Non- ST segment elevation myocardial infarction (NSTEMI) in the
setting of thrombocytosis and multiple admissions for menorrhagia and epistaxis in the setting of
thrombocytopenia. Laboratory work up showed a platelet count of 996k/mm3, troponin of 1.83 ng/ml
which peaked at 3.89 ng/ml. Antiplatelet and anticoagulation therapy were initiated. A bedside
echocardiogram showed normal ejection fraction and no regional wall motion abnormalities.
Subsequently, coronary angiography suggested no epicardial coronary obstruction and CT angiogram of
the chest was negative for pulmonary embolism. She was diagnosed with NSTEMI presumptively related
to microvascular thrombosis in the setting of profound thrombocytosis. Eltrombopag was held and her
dose was reduced from 50 mg to 12.5 mg before discharge. Decision was made to start patient on
prophylactic enoxaprin during any future episodes of profound thrombocytosis and to stop low dose
aspirin if platelet counts drop below 50K.
DISCUSSION: Eltrombopag, a Thrombopoietin receptor (TPOr) agonist, is an FDA approved treatment for
refractory immune thrombocytopenic purpura. Common side effects include; headache, anemia, and
fatigue. Hepatotoxicity is a relative contraindication for use and thromboembolic events have been
reported as a complication. A recent metanalysis showed a trend towards increased risk of
thromboembolism with the use TOPr agonists but this was not statistically significant . Moreover,
Eltrombopag use in patients with chronic liver disease was associated with an increased incidence of
portal-vein thrombosis, as compared with placebo. To our knowledge, this is the first reported case of
recurrent myocardial infarctions with the use of this medication.
[Date]
CONCLUSION: Eltrombopag related thrombocytosis can precipitate myocardial infarction through a
speculated microvascular thrombosis. This complicates the treatment of ITP patients.
71
MICHIGAN PODIUM PRESENTATION - CLINICAL VIGNETTE Jandark Yuseif, MBchB
Chicken Pox, as the initial presentation of hairy cell leukemia.
First Author: Jandark Yuseif, MBchB Omar Al-Shuwaykh M.D. Talin Nemri M.D Dahlia Sano M.D.
Sonikpreet Aulakh M.D. Zain Kulairi M.D.
Objective: Recognize adult onset chicken pox as the initial manifestation of underlying lymphoproliferative disorder.
Introduction: Varicella Zoster Virus (VZV) is one of the herpes viruses. It is known to cause chicken pox
in children and young adults; and shingles (herpes zoster) in adults and very rarely in children. It has
been reported that patients with Lympho-proliferative disorders experience higher rates of VZV
infection.
We are reporting a case of adult Chicken Pox as the first manifestation of hairy cell leukemia. To our
knowledge, this is the first reported case.
Case presentation: A 61 year-old previously healthy male, with no prior history of chicken pox infection,
or vaccination. Came in to the hospital complaining of diffuse skin rash of five-day duration. The rash
started as papular on the lower back, then it spread to the rest of his body sparing the palms and soles.
The rash progressed from papular into vesiclular that crusted few days later. No splenomegaly could be
identified on physical exam. His blood work revealed WBC count of 1800 cells/mcl, platelet count of
100,000 cells/mcl, and hemoglobin of 12 grams/dl. Patient was started on intravenous acyclovir with
daily follow up on his complete blood count. Over the next few days, the rash started to crust and
resolved gradually, but the WBC count decreased to 1400 cells/mcl, and then to 1200 cells/mcl.
The decision was made to proceed with bone marrow biopsy. The flow cytometric immunophenotyping
identified a monoclonal B-cell population expressing CD20, CD25, CD103, CD11c and negative for CD5
and CD10.and positive Tartrate-resistant acid phosphatase. Which confirmed Hairy cell leukemia
diagnosis.
[Date]
Discussion: Hairy cell leukemia is an uncommon chronic lymph proliferative disorder. It accounts for 2%
of all leukemia. The classic manifestations of HCL are abdominal fullness or discomfort due to
splenomegaly, systemic complaints, such as fatigue, weight loss, bruising, bleeding secondary to
thrombocytopenia, or recurrent infections. One quarter of patients are generally asymptomatic and
come to the clinician's attention because of incidentally found splenomegaly or
pancytopenia. Literatures search described the occurrence of opportunistic infections (e.g. Candida,
mycobacria, and Cryptococcus), viral infections (e.g. herpes simplex, cytomegalovirus, and hepatitis
virus) and various bacterial infections in HCL. Varicella zoster infection as the first manifestation of HCL
was not reported before according to our literature search. Our goal for reporting this case is to increase
awareness of potential underlying lymphoproliferative disorder, specifically, hairy cell leukemia for Adult
Patients presented with disseminated varicella zoster.
72
MINNESOTA PODIUM PRESENTATION - CLINICAL VIGNETTE Jennifer Chang Chieh Yui, MD
Serotonin Syndrome in Single Agent Bupropion Overdose
First Author: Jennifer Chang Chieh Yui, MD Ana Zamora Martinez, MD
Introduction: Serotonin syndrome is a potentially life-threatening condition resulting from the
overstimulation of serotonin receptors in the central nervous system. Presentation features mental
status changes, autonomic hyperactivity, and neuromuscular abnormalities.
Bupropion is a dopamine and norepinephrine reuptake inhibitor, without any direct serotonin
action. Thus, its ability to precipitate serotonin syndrome has been challenged. Below, we present a
case of single agent bupropion overdose, with resultant serotonin syndrome.
Case Presentation: A 17 year-old female with poorly controlled depression was being treated with
bupropion monotherapy. The day of admission, she got into a heated argument with family and
ingested 23 tablets of bupropion 300 mg. After having a seizure at a local ED, she was brought to our
medical ICU. After admission, she had two further myoclonic seizures and a witnessed aspiration event.
She was emergently sedated and intubated. Ampicillin-sulbactam was initiated to treat aspiration
pneumonia.
Per her family’s report, there were no other co-ingestions, and urine drug screen was positive only for
THC. She was started on levetiracetam for seizure prophylaxis, and intravenous propofol was required to
control her severe agitation. Her myoclonus persisted despite levetiracetam treatment, and EEG
showed diffuse slowing but no correlating epileptiform discharges. She was intermittently febrile, with
highest temperature 38.8 C. The following morning, she was noted to have ocular myoclonus and axial
rigidity.
She was diagnosed with serotonin syndrome and initiated on cyproheptadine therapy. Within 24 hours
of initiating treatment, physical signs of serotonin syndrome had resolved. Her agitation also resolved,
and she was extubated. She was transferred out of the ICU and weaned off cyproheptadine over the
next three days. Once medically stable, she was admitted to an inpatient psychiatry unit.
Discussion: Bupropion has often been implicated as a contributing cause in multi-agent overdoses
causing serotonin syndrome. However, the serotonergic action of bupropion has been debated and
generally felt to be nonsignificant based on animal trials and very small in vivo trials.
[Date]
In this case, the clinical presentation and resolution of symptoms after treatment with cyproheptadine
certainly point toward serotonin syndrome. The Hunter criteria for diagnosis of serotonin syndrome
feature the initial qualifier of the presence of a serotonergic agent. While bupropion is not a direct
serotonergic agent, perhaps this agent’s mechanism and its interaction with serotonin in vivo needs to
be further elucidated to clarify it as a potential cause of serotonin syndrome in single agent overdose.
73
NEW YORK PODIUM PRESENTATION - CLINICAL VIGNETTE Dilasha Katwal, MD
West Nile Virus Induced Opsoclonus-Myoclonus Syndrome
First Author: Dilasha Katwal, MD 1 Eric Sklar MD2, Rashmi Banjade MD1 , Stephen Jesmajian MD1 1
Montefiore New Rochelle Hospital and Albert Einstein College of Medicine, New Rochelle, New York. 2
Inova Fairfax Hospital, Falls Church, Virginia
Opsoclonus–Myoclonus–Syndrome (OMS) is a rare neurological disorder consisting of involuntary,
chaotic, multidirectional saccades without inter-saccadic intervals known as opsoclonus and arrythmicaction myoclonus predominantly involving the trunk and the neck. It may be associated with a
paraneoplastic syndrome or may occur due to toxins, autoimmune diseases, infections, or idiopathic in
origin. We present a case of West Nile Virus infection presenting with OMS.
A 51 year old female presented with diffuse headache of two days associated with abnormal movement
of her eyes and difficulty in focusing on objects. She also had difficulty ambulating due to dizziness and
worsening right upper extremity tremor. On the day her symptoms started, she had noticed pink, nonpruritic rash on her chest, abdomen, and arms that resolved spontaneously. She had intermittent chills
but no fever. She denied any recent travel, insect bites, sick contacts, new medication or drug use. She
had a family history of lung cancer in both her parents and thyroid and renal cancer in a brother. She
was a non-smoker. On admission, she was afebrile and her vitals were stable. She was alert and
oriented. Meningeal signs were absent. She had small-amplitude rapid, involuntary, horizontal and
vertical eye movements, which was slightly suppressible with her forced gaze. Tremor was noted with
postural extension of right arm. Gait was deferred. Other neurological and systemic exams were
unremarkable. Her complete blood counts, complete metabolic panels, erythrocyte sedimentation rate,
thyroid-stimulating hormone, chest x-ray, and collagen vascular disease antibody panel were normal or
negative. CT scan head, CT angiogram head and neck, MRI head, CT scan chest, abdomen and pelvis with
contrast, transvaginal ultrasound pelvis, bilateral digital mammogram and paraneoplastic antibodies
were all negative. HIV, Lyme disease, group A streptococcus, influenza tests were negative. Lumbar
puncture revealed CSF with WBC of 11 with 37% neutrophil, 33% lymphocytes and 30% monocytes,
glucose 54mg/dl and protein 56mg/dl. CSF HSV PCR, CMV, EBV, bacterial cultures were all negative.
Serum West Nile Virus IgM antibodies were positive and IgG antibodies were negative. Patient was
symptomatically managed with Clonazepam and Topiramate, which improved her opsoclonus and
myoclonus gradually, and she was eventually discharged to a rehabilitation facility. During one month
follow up, she had occasional opsoclonus and myoclonus and mild postural tremor.
[Date]
OMS is a rare autoimmune condition characterized by cerebellar degeneration seen in patients
secondary to various etiologies like cancers, toxins, autoimmune diseases, and viral infections. It is
important to rule out malignancy on adult patients with OMS especially presenting with encephalitis.
Therefore, our initial investigations were focused to rule out different types of tumors associated with
OMS like breast cancer, small cell lung cancer and gynecological cancers. Our extensive investigation
eventually diagnosed WNV encephalitis, which is an unusual cause of OMS with only a few reported
cases so far.
74
TEXAS PODIUM PRESENTATION - CLINICAL VIGNETTE Alfredo Camero Jr, MD
Classic Hypertensive Emergency? An Unusual Case of Labile Hypertension
First Author: Alfredo Camero Jr, MD Second Author: Kanapa Kornsawad, MD
Case Presentation: A 65 year-old man presented with 1 day of headaches and dizziness. He denied
vision changes, chest pain, or weakness. His past medical history was significant for hypertension,
chronic kidney disease stage III, and type 2 diabetes mellitus. His blood pressure was noted to be
216/122 with otherwise normal vital signs. His physical exam demonstrated no neurologic abnormalities
and his optic disc showed no papilledema. His serum creatinine was 3.7 mg/dL with a baseline serum
creatinine of 1.6 mg/dL. A computed tomographic scan of his head was normal. He was started on a
nicardipine drip for aggressive blood pressure control. His blood pressure was labile and corrected
quickly over 1 hour to 140/80, and thus the drip was stopped. His blood pressure remained labile
throughout the subsequent days. On his third hospital day, he developed altered mental status with
hypercapnea that required intubation. It was then noted that he could not move his extremities but did
open and close his eyes on command. His physical exam at that time showed areflexia. A magnetic
resonance image of the brain showed a small acute lacunar infarct involving the left lateral thalamus,
which did not explain his neurologic deficits. Lumbar puncture was performed due to a concern for
Guillain Barre Syndrome (GBS). Cerebrospinal fluid studies showed a protein level of 144 mg/dL
(elevated), no white blood cells, and a negative infectious workup. Electromyography (EMG) and nerve
conduction studies were performed that showed evidence of primarily axonal sensory/motor peripheral
polyneuropathy. His autoimmune workup was significant for a positive antibody to ganglioside GM1.
These results were consistent with a diagnosis of acute motor and sensory axonal neuropathy (AMSAN),
a variant of GBS. He was treated with IVIG therapy with remarkable improvement and eventual full
motor recovery.
[Date]
Discussion: Dysautonomia is a common feature of GBS (reported as high as 70% of cases). Typical
cardiovascular findings of dysautonomia in GBS include tachycardia, persistent hypertension, labile
blood pressure, or arrhythmias. Although his labile blood pressure was a clue of dysautonomia, he
wasn’t experiencing neurologic symptoms yet, so a disease like GBS was not on our differential
diagnosis. AMSAN is a variant of GBS typically seen in non-US countries. This variant of GBS is typically
differentiated via EMG and antibody tests anti-gangliosides and is associated with higher rates of
respiratory failure. Our case highlights a very unusual clinical presentation to an atypical variant of GBS.
Hypertensive crises that are overly labile should raise the suspicion to a general internist of the
possibility of dysautonomia playing a pathophysiological role and thereby adjusting their differential
diagnoses accordingly.
75
TEXAS PODIUM PRESENTATION - CLINICAL VIGNETTE Vineet S Gudsoorkar, MBBS
Pay Heed to Weed: It’s a diagnostic lead and a public health need!
First Author: Vineet S Gudsoorkar, MBBS Second Author: Jose A. Perez Jr. MD, FACP
Introduction: Synthetic cannabinoids (SCs) are blends of plant material with varying concentrations of
synthetic analogues of cannabinoids sold as incense or potpourri, labeled “Not for human use”.
However the magnitude of SC abuse is rapidly increasing, especially among the young adults. These
products can be easily ordered on the internet. Renal failure is a rare complication associated with SC
abuse. We describe a case of acute kidney injury (AKI) associated with use of SCs and their impact on
public health.
Case Description: A 26 year-old male was brought to the emergency department (ED) after a seizure-like
activity. He was intubated on arrival. His family reported that he had been in his usual health until the
symptom onset, and had been smoking “synthetic weed” for the previous 2 days including the night
prior to admission.
Physical examination revealed a well nourished male on mechanical ventilation with normal vital signs
and the remainder of physical examination.
The laboratory studies showed a creatinine of 2.3 mg/dl, BUN of 25 mg/dl and a CPK of 2337 units/liter.
A urinalysis showed 5 RBC/HPF, normal myoglobin levels, 1+ proteinuria, and no white blood cells or
casts were seen. The fractional excretion of sodium was 5.09. Renal ultrasound revealed a normal
echotexture and size. No other hemodynamic, infectious, pharmacologic or autoimmune etiology of
renal failure was found. His creatinine peaked at 8.1 mg/dl on day 4 and then began to improve with
supportive treatment. It was 2 mg/dl upon discharge with complete resolution of electrolyte
abnormalities. His urine output remained above 0.5 ml/kg/hour throughout his hospitalization.
Discussion: Renal toxicity of SCs has been reported in 21 cases, prompting a CDC alert. All patients had
improvement in renal function over a variable time course. The pathogenesis of renal involvement
remains unclear, but may involve the toxic metabolites- XLR11 or UR144. The serum and urine assays to
detect SCs and their metabolites are expensive and not easily available. Fifty-one new SC compounds
were identified in 2012, compared to just two in 2009. SCs were implicated in 11,400 ED visits in 2010,
75% of which were in the age group of 12-29 years. One in nine 12th graders in the USA reported using
SCs in the past year. However, many ED physicians feel unprepared to treat these patients.
Conclusion:
[Date]
1. SC abuse is a significant public health hazard, and a new differential diagnosis of AKI in young
adults.
2. If a clear history of SC abuse preceding the AKI is available, invasive diagnostic studies may be
deferred.
3. It is potentially reversible with supportive treatment, although the long term effects are
unknown.
76
TEXAS PODIUM PRESENTATION - CLINICAL VIGNETTE John Hunninghake, MD
Arterial Thrombus and Myocardial Infarction after Discontinuation of a Novel Oral
Anticoagulant in a Patient with Protein C Deficiency
First Author: John C. Hunninghake, MD Second Author: Hugh M. Coke, MD Third Author: Gilberto Patino,
MD Fourth Author: Jamil A. Malik, MD
Introduction: Protein C deficiency is a disorder of the coagulation cascade resulting in a hypercoagulable
state that puts a carrier at risk for venous thromboembolism. Certain studies have suggested a
correlation of this disorder with arterial thrombosis, especially within the coronary vasculature. Multiple
case reports have described acute myocardial infarction in young patients as the presenting syndrome
for protein C deficiency; however, no case reports describe a patient who had been treated with a novel
oral anticoagulant (NOAC) for secondary DVT prevention.
Case Report: The patient is a 23 year old male with a history of a pulmonary embolus (PE). After
completion of a 6-month course of coumadin as treatment for the PE, his hypercoagulability workup
was positive for protein C deficiency. He was subsequently started on rivaroxaban with instructions to
continue lifelong as secondary prevention for recurrent DVTs. Three months later, he stopped his
rivaroxaban due to initiation of an exercise regimen shortly after arriving to San Antonio from a crosscountry road trip. Three weeks later, he presented to the ED with a 2 day history of pleuritic chest pain
and dyspnea on exertion. CT angiogram was negative for acute pulmonary embolus, but his initial
troponin-T was elevated (0.19 ng/mL) with T-wave inversions on EKG. Due to concern for ACS, he was
taken to the cardiac catheterization lab for angiography of both his pulmonary and coronary arteries. A
massive thrombus was discovered in the proximal-to-mid LAD with no significant atherosclerosis. He
underwent aspiration and mechanical thrombectomy. Post-procedure, he was started on yearlong dual
antiplatelet therapy for secondary MI prevention for NSTEMI due to the uncertainty of plaque rupture
contribution. For the hypercoagulable state attributed to protein C deficiency, systemic anticoagulation
was restarted with lifelong coumadin and a short LMWH bridge due to his temporary hypercoagulable
state. Other than mild mucosal bleeding and a small retroperitoneal hematoma, the patient remained
hemodynamically stable for the remainder of the hospitalization with no recurrent angina symptoms.
[Date]
Discussion: Certain NOACs have been approved for secondary DVT prevention; however, no literature
was found that addresses their risk reduction for venous or arterial thromboembolism specifically in
protein C deficiency. This case questions whether the discontinuation of a NOAC contributed to a
hypercoagulable state that predisposed a high-risk individual to the development of a significant
coronary arterial thrombosis. Further investigation is necessary to evaluate the safety of NOACs as
secondary DVT prevention in protein C deficiency.
77
VIRGINIA PODIUM PRESENTATION - CLINICAL VIGNETTE Nathaniel C Warner, MD
Look What the Cat Dragged In: An Unusual Case of LVAD-associated Endocarditis.
First Author: Nathaniel C Warner, MD
Mr. H is a 69-year-old Caucasian gentleman with history of severe ischemic cardiomyopathy status post
aortic valve replacement and left ventricular assist device (LVAD) who developed vague symptoms of
fatigue and malaise. Initially, his symptoms were attributed to worsening heart failure, so he underwent
right heart catheterization, which showed unchanged post capillary pulmonary hypertension. His
symptoms continued for two months, until he mentioned daily low-grade fevers without other localizing
symptoms to his outpatient cardiologist. Computed tomography of the chest was obtained to evaluate
for VAD malfunction or occult abscess but imaging was unrevealing.
Four months after initial symptom onset, the patient noted a fever to 100.8. Two days later, routine labs
revealed acute renal failure (Cr 3.29 mg/dL) and the patient was admitted to the hospital for further
workup. On admission, the patient was a well appearing middle-aged gentleman in no acute distress. He
was afebrile and his vital signs were stable. Physical examination was unremarkable including LVAD hum
and normal appearing driveline. There were no rashes. Laboratory data was significant for new
pancytopenia and acute renal failure.
Blood cultures were drawn and TEE showed no obvious vegetation. Further detailed history revealed
that the patient had two cats, including a new kitten, which frequently scratched him while playing.
Given his exposure history, serologies were drawn for Bartonella henselae, Bartonella quintana and
Coxiella burnetti in addition to blood cultures.
Five days later, B. henselae IgG returned strongly positive (1:2560) and the diagnosis of LVAD-associated
B. henselae infective endocarditis was made. Due to the patient’s acute renal failure, an aminoglycoside
sparing regimen was used consisting of ceftriaxone, doxycycline, and rifampin for six weeks followed by
doxycycline through cardiac transplantation. The patient was relisted for heart transplant, and three
months later, underwent successful cardiac transplantation. Over one year later, he remains well
without complication or recurrence of infection.
[Date]
Discussion: Bartonella henselae is a small, aerobic gram negative bacillus known to cause a spectrum of
illness depending on risk factors and immune status of the host. Classically, it is known to cause focal,
suppurative disease in the immunocompentent, and multifocal, disseminated disease in the
immunodeficient. It is also a well known cause of blood culture negative endocarditis. Its prevalence
varies by region from 1-15% and is associated with feline exposure and preexisting valvular disease.
Aminoglycoside therapy is the treatment of choice in these patients, but was not possible in this patient
due to acute renal failure. This appears to be the first case of LVAD-associated Bartonella hensalae
endocarditis described in the literature and emphasizes the importance of a detailed history when
evaluating suspected infective endocarditis.
78
[Date]
RESIDENT FELLOW VIGNETTE POSTER FINALSTS
79
ALABAMA POSTER FINALIST - CLINICAL VIGNETTE Ashley E Jackson, MD
Spontaneous native aortic valve thrombosis: a rare case teaches vital medical
points
First Author: Ashley E Jackson, MD, UAB Internal Medicine residency, Huntsville campus, AL. Ali B
Hachem, MD, The Cancer Center of Huntsville, AL. Richard C Clay, MD, Huntsville Cardiothoracic
Surgeons, AL. Navdeep K Mann, MD. Heart Center, Inc. AL.
INTRODUCTION: Even though spontaneous native aortic valve thrombosis is an extremely rare
phenomenon, it can be suspected with simple yet thorough physical exam. We report an unusual
presentation of this rare diagnosis.
CASE : A 32-year-old African American male presented ER with acute, severe right leg pain, numbness,
and weakness while cutting grass. Physical exam demonstrated right lower extremity pallor, cool skin
temperature, absent sensation, weak femoral pulse, and absent pedal pulses. Arterial Doppler and CTA
confirmed right common iliac arterial occlusion and incidental splenic and renal infarcts. Labs at
presentation showed Hb of 22.3 and Hct 63.8, WBC 19,660, and platelets 25,000. Record review showed
patient had been diagnosed 6 years back with polycythemia rubra vera (PRV) JAK2 negative; however,
he was lost to follow-up due to lack of insurance. Vascular surgeon performed urgent thrombectomy to
reduce critical limb ischemia, successfully restored blood flow, performed therapeutic phlebotomy, and
placed patient on aspirin and heparin. Hematology was consulted and found a crescendo-decrescendo
systolic ejection and diastolic murmur in aortic area. Thus, 2-D ECHO and TEE were ordered, which
revealed extensive thrombosis of aortic valve (AV) leaflets, severe aortic stenosis and insufficiency, and
concentric left ventricular hypertrophy with preserved ejection fraction. Patient underwent AV
replacement with mechanical valve. Gross examination showed organized clot in right and left cusps
with thrombus extension above the valve to underneath the left main trunk, encircling the right
coronary ostia, and over the anterior leaflet of mitral valve. Microbiology cultures were negative, and
histology confirmed organized thrombus. Patient was discharged on warfarin with therapeutic INR. Two
months after surgery, he is doing well, has insurance, and has continued follow-up.
[Date]
DISCUSSION : This case displays a rare pathology, highlights a barrier to follow-up, and reiterates the
importance of thorough clinical examination. Even though PVR frequently causes isolated acute arterial
thrombosis, a systemic embolic phenomenon should also be considered. In this case, diligent physical
exam and imaging review confirmed such an unusual presentation, which lead to prompt aortic valve
surgical repair, thus avoiding additional catastrophic thrombo-embolism. Unfortunately, patient had
been lost to follow-up since original PRV diagnosis because he was uninsured. That negated any
potential opportunity to medically intervene sooner, and it remains to be a significant barrier to
appropriate healthcare in the United States.
80
ALABAMA POSTER FINALIST - CLINICAL VIGNETTE Sarah R Kunin, MD
Dying for Moonshine: A rare case of copper toxicity
Sarah A. Kunin, MD and Eric Cornatzer
Moonshine has been increasing in popularity since the start of the economic recession in the U.S. There
have been few reports on chronic copper toxicity from consuming moonshine. Most of the current
literature looks at acute copper toxicity, but it has yet to evaluate chronic copper toxicity.
The patient we present is a 65-year-old white male who presented with a history of worsening shortness
of breath, diffuse swelling, and newly diagnosed CHF. The patient had a history of drinking one-fifth of a
gallon daily of moonshine that had toxic levels of copper in it. He developed AKI that rapidly progressed
to ESRD. He had recurrent ascites from his newly diagnosed cirrhosis. He was found to have elevated
levels of copper in his blood at the time of presentation, which was one month after he quit drinking
moonshine. The patient’s cirrhosis and renal failure were due to his alcohol abuse and chronic copper
toxicity from the moonshine.
[Date]
As moonshine becomes more prevalent in popular culture, clinicians need to clarify whether their
patients are consuming moonshine. In addition, clinicians need to think about screening their patients
for heavy metal toxicity, especially if they have a variety of seemingly unrelated symptoms.
81
ARIZONA POSTER FINALIST - CLINICAL VIGNETTE Jawad Bilal, MD
Intravenous Immunoglobulin induced pulmonary embolism: It's time to act!
First Author: Jawad Bilal, MD Second Author: Jennifer L. Hill, MD Third Author: Irbaz bin Riaz, MD Last
Author: Tirdad T. Zangeneh, DO, FACP
INTRODUCTION: Pulmonary Embolism (PE) is a common clinical problem affecting 600,000 patients per
year in United States. Although the diagnosis can be easily confirmed by imaging techniques such as
Computed Tomographic Angiography (CTA) of the chest, the identification of underlying mechanism
leading to PE is important for appropriate duration of anti-coagulation and prevention of subsequent
episodes. The differential diagnosis of underlying mechanism is broad and must include careful review
of medication history.
CASE PRESENTATION:A 57-year-old male with history of hypertension, hyperlipidemia, selective
immunoglobulin G (IgG) deficiency, and treated Hodgkin’s Lymphoma presented with acute onset
shortness of breath. He denied chest pain, palpitations, orthopnea, paroxysmal nocturnal dyspnea,
fever, cough or hemoptysis. He had no history of recent surgery, travel, trauma, cancer, or
immobilization. His medications included aspirin, amlodipine, lisinopril, atorvastatin and Intravenous
venous Immunoglobulin (IVIG). On physical examination, temperature was 38.5 C, blood pressure 135/
85 mmHg, pulse 106/min and respirations 25/min. Lungs were clear and there was no calf tenderness or
swelling. His complete blood count and chemistries were normal. The troponins were elevated without
any ischemic changes on EKG. Hypercoagulability work up including antithrombin III, protein C, protein
S, heparin cofactor II, homocysteine, factor V Leiden mutation, and antiphospholipid antibodies was
normal. CTA of the chest revealed bilateral pulmonary emboli involving upper, middle and lower lobe on
the right side and upper and lower lobe on the left side. Lower extremity Doppler venous ultrasound
revealed deep vein thrombosis in lower legs bilaterally. He received low-molecular-weight heparin and
was transitioned to warfarin anticoagulation.
Discussion: Woodruff et al. first reported thrombotic complications of IVIG in 1986. In last two decades,
the incidence and determinants of IVIG-related thrombotic complications were not well established. It is
unclear if factors such as sex, race, indication, dose or duration of IVIG therapy independently increase
the thromboembolic risk. It is thought that IVIG related thromboembolic disease occurs within 30 days
of administration of IVIG. This patient developed pulmonary embolism 3 days after administration of 40
g of IVIG. The pathogenesis is poorly understood but increased blood viscosity, activation of platelets
and clotting mechanisms, arterial vasospasm, disruption of atherosclerotic plaques, and in situ
thrombosis have been implicated.
[Date]
In patients receiving IVIG, the risk for thromboembolism should be emphasized. Steps should be taken
for risk stratification and monitoring the risk of thromboembolic complications in these patients. This
patient developed PE despite being on aspirin. The role of prophylactic anti-coagulation especially in
patients at high risk of thromboembolism at least for the duration of therapy should be addressed. Risk
and benefits of IVIG therapy should be carefully considered before initiation of therapy in patients with
high risk of thromboembolism.
82
ARIZONA POSTER FINALIST - CLINICAL VIGNETTE Melissa A Crawley, MD
In a Pickle: Foodborne Botulism
First Author: Melissa A Crawley, MD Second Author: Mayar Al Mohajer
Adult foodborne botulism is a rare toxin-mediated illness characterized by bulbar paralysis and
descending neuromuscular weakness. This case illustrates the necessity of prompt recognition and
empiric administration of antitoxin to limit further progression of symptoms.
A 40-year old man was admitted with a chief complaint of slurred speech, difficulty swallowing, and
double vision. He awoke that morning able to eat with some difficulty swallowing. As the day
progressed, he had difficulty speaking, and developed diplopia. By the time he arrived at the hospital, he
was not able to speak or swallow. History was obtained by the patient’s fiancé, who noted that two days
prior to presentation, the patient ate home-canned pickles that tasted foul.
On examination, his vital signs were normal. His neurological examination was remarkable for severe
dysarthria with minimal tongue movement, and inability to protrude his tongue past his teeth. His pupils
were equal, round, and sluggishly reactive to light, and his extraocular movements were minimal in all
directions. He had bilateral ptosis and facial weakness. Shoulder shrug strength was normal. Palate
elevated symmetrically. The remaining examination was unremarkable.
Differential diagnosis on admission included foodborne botulism, variant Guillain-Barre syndrome, and
myasthenia gravis. Initial laboratory evaluation, including complete metabolic panel, complete blood
count, urinalysis, and blood and urine cultures, was unremarkable. Cerebrospinal fluid analysis, including
culture, was unremarkable. Ganglioside GQ1b and West Nile Virus antibodies were
negative. Acetylcholine receptor antibody testing was negative. MRI of the brain was normal.
The patient was admitted to the ICU and intubated for airway protection. Given his clinical presentation
and high suspicion for food-borne botulism, he was treated empirically with a single dose of equine
heptavalent botulinum antitoxin. Stool and serum specimens, as well as the pickles implicated in the
initial history, were collected and sent to the Centers for Disease Control and Prevention for
analysis. Serum botulinum bioassay returned with a positive result for Botulinum type B. No further
progression of his paralysis occurred, and he improved throughout his hospital course. Extubation
occurred after eleven days and he was discharged to inpatient rehabilitation.
[Date]
Adult foodborne botulism results from ingestion of preformed botulinum toxin, usually from improperly
home-canned foods. The toxin inhibits acetylcholinesterase release from presynaptic receptors,
resulting in acute bilateral cranial neuropathies, often with blurred vision, involvement of cranial nerves
III, IV, or VI, and with symmetrical descending weakness. Respiratory failure occurs with upper airway
dysfunction or diaphragmatic weakness. Diagnosis is achieved with a mouse bioassay, and requires
confirmation of the presence of toxin in serum, gastric secretions, stool, or food samples. Treatment
with botulinum antitoxin may reduce duration and severity by limiting further progression of symptoms,
but does not reverse existing symptoms.
83
ARIZONA POSTER FINALIST - CLINICAL VIGNETTE Kyle J Henry, MD
Large B Cell Lymphoma presenting as Bilateral Lower Extremity Pain,
Asymptomatic Pericarditis and Pericardial Effusion
First Author: Kyle J Henry, MD Sandra L Till, DO Michael S Chesser, MD Clement U Singarajah, MBBS
Felipe Gutierrez, MD Kristine Saunders, MD
We present the unexpected death of a 66 year old man from cardiac tamponade caused by a malignant
effusion from B cell lymphoma. He presented to the hospital complaining of four months of
progressively worsening and debilitating foot pain radiating to his legs.
Initial physical exam findings were mostly unremarkable. He was noted to be obese and had lower
extremity edema to the knees bilaterally. Pericardial friction rub was barely audible on presentation, but
easily discernable the day after. An ECG revealed diffuse concave ST-elevations concerning for
pericarditis. Labs revealed negative cardiac biomarkers, but were significant for anemia, elevated
inflammatory markers, and acute renal failure. Peripheral smear was unrevealing. The patient was
admitted for further evaluation. His lower extremity pain completely resolved with pain medications
and diuretics on hospital day 1. An echocardiogram confirmed a pericardial effusion with evidence of
mild tamponade physiology. Given these findings, the patient was transferred to the Intensive Care Unit
for closer monitoring. Later that day, he developed atrial fibrillation and was started on a heparin drip.
The patient's acute renal failure progressed, requiring initiation of hemodialysis. Splenomegaly was
incidentally noted on renal ultrasound, prompting further imaging with a CT Chest/Abdomen/Pelvis that
demonstrated diffuse lymphadenopathy. Daily bedside echocardiograms and another official
transthoracic echocardiogram repeatedly demonstrated stable pericardial effusion with mild tamponade
physiology. CT-guided lymph node biopsy findings were nonspecific. Excision lymph node biopsy was
scheduled.
On hospital day 12, the patient described malaise and nausea, and was noted to have decreased blood
pressures. He later suffered cardiac arrest, and initial advanced cardiac life support resulted in return of
spontaneous circulation. Bedside echocardiogram post-cardiac arrest revealed significant increase in
pericardial fluid and tamponade physiology. An emergent ultrasound-guided bedside pericardiocentesis
was performed revealing frank blood with removal of 60cc of pericardial fluid. While preparing
the patient for cardiothoracic surgery he developed massive thoracic cavity bleeding and could not be
resuscitated. Pathologic examination of the pericardiocentesis fluid finally diagnosed Large B Cell
Lymphoma.
[Date]
B Cell Lymphoma with cardiac involvement is a rare entity. This case is especially remarkable given the
initial asymptomatic presentation of his pericarditis and demonstrates that a malignant effusion can
quickly develop fatal tamponade with anticoagulation.
84
ARIZONA POSTER FINALIST - CLINICAL VIGNETTE Edward R Maharam, MD
Improving Sepsis & Worsening Hypoglycemia? A Case of Levofloxacin Associated
Hypoglycemia.
Edward R Maharam, MD, Mark R Pedersen, MD, Adam Bosak, MD, Sathya G Jyothinagaram, MD, MRCP,
FACE
Purpose: The quinolone class of antibiotics, including levofloxacin, is rarely associated with severe
hypoglycemia (0.1-1%).
Case: A 62 year old male with a history of end stage renal disease on hemodialysis with limited vascular
access and no history of diabetes who was hospitalized for management of pneumonia and a
Pseudomonas line infection. His initial antibiotic regimen included levofloxacin 500 mg every 48 hours.
Within two hospital days, he had episodes of mild hypoglycemia. On day three, he was started on a D10
drip. Meanwhile, he was afebrile with decreasing leukocytosis from 10.4 to 6.8. At one week
hospitalization, blood glucose (BS) nadir was 36, with frequently dropping into the 40s and 50s,
requiring D10 at 40 ml/hour. He was transferred to our facility for endocrinology evaluation.
On presentation, he was confused with a blood glucose of 41. His confusion improved with intravenous
dextrose. He remained persistently hypoglycemic. D10 was up titrated to 125 ml/hour then switched to
D20. Overnight, 6 ampules of D50 were required. C Peptide was 15.2 ng/ml while blood sugar was 73.
Labs included WBC of 7.0, Sodium of 114, Potassium of 4.8, Creatinine of 9.41, free T4 of 1.0. The only
immediate intervention was discontinuing levofloxacin and a one-time dose of octreotide followed by
dialysis. Then, the dextrose-containing fluid was stopped, and hypoglycemia did not recur.
Discussion: This patient’s hypoglycemia was multifactorial, likely related to malnutrition and sepsis
(persistent Pseudomonas bacteremia), but also likely engendered by levofloxacin. He had multiple risk
factors for developing hypoglycemia on levofloxacin, including the aforementioned causes, as well as his
older age and end-stage renal disease. The mechanism of levofloxacin induced hypoglycemia is thought
to be similar to that of a sulfonylurea, inhibiting ATP-sensitive K+ channels on ß-cells, and thereby
releasing insulin, leading to hyperinsulinism. This is similar to what we observed –high C-peptide levels
during a period of relative hypoglycemia. The problem resolved with the administration of octreotide
(decrease insulin release), dialysis and discontinuation of levofloxacin.
[Date]
Levofloxacin and the quinolones are commonly known for their effect of prolonging the QT interval,
causing Clostridium difficile-associated diarrhea, and potential hepatotoxicity, but their effect on
hypoglycemia is relatively less well known. A survey of 97 clinicians in the United Kingdom
demonstrated that 79 (80.4%) were unaware that levofloxacin could cause hypoglycemia. This case
demonstrates levofloxacin-induced hypoglycemia, a rare side effect associated with all quinolones. It
should be considered in patients on these antibiotics who present with low blood sugars without other
clear cause.
85
ARIZONA POSTER FINALIST - CLINICAL VIGNETTE Geoffrey J Orme, DO
Post-gastric bypass hypoglycemia with bulimia nervosa: An even more frustrating
disorder
Joseph Orme DO, MPH Vijayaratna Chockalingam MD Cheryl O'Malley MD Brenda Shinar MD, RIchard
Gerkin MD
Introduction: Post-gastric bypass hypoglycemia (PGBH) complicates approximately 0.1-0.36% of cases status post
Roux-en-Y surgeries. It is a complicated and frustrating disease to manage, for health care providers, and patients .
To further complicate the diagnosis and management of such a disease, this is the first documented case report of
a patient with PGBH who also suffers from borderline personality disorder and severe bulimia nervosa.
Case presentation: A 33-year-old female, former ICU nurse, with a past medical history of obesity status post
Roux-en-Y gastric bypass performed 11 years prior to presentation. She had a history of several previous
hospitalizations requiring enteral tube feeding. She was transferred to our facility from an inpatient treatment
center for evaluation of severe recurrent postprandial hypoglycemia. Although factitious hypoglycemia was
suspected, laboratory results were suggestive of an endogenous hyperinsulinemic hypoglycemic etiology. At the
time a serum blood glucose level was 26mg/dl, her serum insulin, C-peptide, and pro-insulin levels were 24µU/ml,
6.8ng/ml and 27.8?mol/l, respectively, along with negative serum insulin antibodies or plasma sulfonylurea. A CT
scan of the abdomen was performed but did not reveal any pancreatic lesions. As the patient continued to have
hypoglycemic events despite conservative dietary changes and medical therapy, an endoscopic ultrasound (EUS)
was performed revealing two 1cm x 1cm lesions in the body and tail of the pancreas that were suggestive of
neuroendocrine origin. Fine needle aspiration (FNA) of each lesion was performed. Pathology did not reveal any
neuroendocrine cells suggestive of insulinoma.
To confirm our hypothesis that her beta-cells were hyperfunctioning, a selective arterial calcium-stimulation test
was performed. Sampling from the gastroduodenal, mid and proximal splenic arteries disclosed diffusely elevated
levels of insulin production throughout the pancreas. This finding proved diffuse beta-cell hyperfunctioning
resulting in hyperinsulinemic hypoglycemia from beta cell hyperplasia. Medical management for this condition
consists of dietary changes (small frequent meals) and either oral or subcutaneous medications. However, in
refractory cases, a partial or total pancreatectomy may be warranted.
Unfortunately, the patient continued to fail conservative medical therapy in part due to her fear of gaining weight
and of needles. The nursing staff had a suspicion that the patient was purposefully disposing of her oral
medications. Furthermore, the patient expressed that she would rather risk undergoing complicated surgical
resection of the pancreas than adhere to dietary changes including small, frequent meals because of her obsession
of weight gain. Once nursing staff directly observed the patient taking her medications, she remained euglycemic
with conservative management.
[Date]
Conclusion: PGBH is a rare complication of bariatric surgery which results in recurrent postprandial hypoglycemia.
Concern for factitious etiology of hypoglycemia in patients with mental illness is warranted, but tremendously
complicates the diagnosis and therapy of this organic cause of hypoglycemia. A multidisciplinary approach
including close observation by nursing staff and careful medical decision-making is paramount.
86
ARIZONA POSTER FINALIST - CLINICAL VIGNETTE Namit N Rohant, MD
The Ancient Disease Scurvy: A Medical Mystery in the Modern World Secondary to
Celiac Disease
First Author: Namit N Rohant, MD
Scurvy, a manifestation of vitamin C (ascorbic acid) deficiency, is a collagen synthesis disease with
numerous variable symptoms including bleeding disorders, malaise, arthralgias, weakness, and so on
that tends to mimic copious other diseases. It was fairly common and well described in the ancient
cultures of Egypt, Greece, and Rome. However, in the modern world, it has become increasingly rare
due to vitamin C fortified foods and fresh fruits and vegetables available to today’s consumers, resulting
in some difficult diagnostic dilemmas.
A 53-year-old gentleman with a medical history of an unknown vasculitis, abdominal aortic aneurysm
repair, brain aneurysm with transient ischemic attack, peripheral neuropathy, transient atrio-ventricular
block, pericarditis, hypertension, and psoriasis presented to the hospital with complaints of fatigue and
weakness for 4 days prior to admission. These symptoms were associated with increasing bruising in his
bilateral proximal lower extremities also occurring for the same time period. He denied any trauma and
was not on any anticoagulation or anti-platelet medications. He also reported chronic myalgias in his
lower extremities. Physical examination on admission was significant for large echhymoses, mild
swelling, and diffuse tenderness in his bilateral lower extremities as well as petechiae over his lower
extremities and left upper extremity. The initial lab work revealed a hemoglobin of 6.3 requiring blood
transfusion. In the setting of his presenting complaints and initial lab findings, a detailed workup for
vasculitis was done due to the patient’s past medical history. The workup included imaging studies,
rheumatoid/hematology labs, infectious/malnutrition labs, as well as biopsies of the skin lesions and
muscles. Multiple services were also consulted for their expert opinion. Lab work eventually revealed
that he had a vitamin C deficiency with plasma levels <5 umol/L.
He was treated for scurvy with vitamin C 500mg IV Q12H for 5 days and was later switched to PO
maintenance dose. His symptoms were noted to markedly improve with time. Upon further discussion
with him, it was revealed that he had been eating a balanced diet with fresh food as well as packaged
fortified foods, making dietary deficiency of vitamin C unlikely. Further investigation revealed that the
patient was positive for celiac disease screen and tissue transglutaminase IgA antibodies, which is
greater than 95% sensitive and specific for celiac disease.
[Date]
This case is particularly unique as the patient presented with scurvy in the setting of celiac disease, an
association that has rarely been described in the literature. Celiac disease is commonly seen today, but it
can result in a multitude of other disorders due to malabsorption of essential vitamins and nutrients.
Additionally, this case demonstrates the importance of having a high degree of clinical suspicion for near
extinct diseases, like scurvy, which can easily be treated once recognized.
87
ARKANSAS POSTER FINALIST - CLINICAL VIGNETTE Jorge L Jo Kamimoto, MD
The Case of the Bound Insulin
Jorge Jo Kamimoto M.D Sandra Susanibar Adaniya M.D. Peter Goulden M.D., F.R.C.P Departments of
Internal Medicine and Endocrinology, UAMS, Little Rock, AR
This case highlights a syndrome where determining the cause of hypoglycemia presents a diagnostic
challenge. A 59 years old male presented to the endocrinology clinic for evaluation of hypoglycemic
episodes characterized by diaphoresis 3 hours after eating. Review of his blood sugar diary revealed
several readings in the 40 to 70 mg/dL range. He had tried snacking between meals without
improvement. He had a history of IgG Kappa Multiple Myeloma and Bone Marrow transplant 9 years
earlier. There was no history of diabetes mellitus. He was not taking any medications which cause
hypoglycemia. Physical exam was unremarkable.
Laboratory evaluation revealed a substantial elevation in random insulin levels, increased C-peptide
levels, and normal glucagon levels. Pancreatic imaging did not reveal any lesions. Concomitantly our
patient had surveillance testing for Multiple Myeloma that revealed an elevation in M protein levels.
Further testing revealed high titers of insulin antibodies, suggesting a diagnosis of autoimmune
hypoglycemia. Our patient was started on a low carbohydrate diet and chemotherapy for Multiple
Myeloma recurrence with Bortezomib and Dexamethasone. A parallel drop was noted in Multiple
Myeloma markers (M protein) and levels of insulin binding antibodies with subsequent resolution of
symptoms confirming the diagnosis.
Hypoglycemia in non-diabetic or non-critically ill patients is a rare event and should trigger further
investigation. In our patient the pattern of hypoglycemia, occurring after meals in the context of a
history of multiple myeloma lead us to suspect a diagnosis of autoimmune hypoglycemia due to
increased insulin antibody production. Previous studies have shown that insulin antibodies have high
capacity and low specificity, this triggers a swift binding of large amounts of insulin during post prandial
peaks (High capacity). Once bound the antibody renders the insulin molecule biologically inactive as it
cannot be absorbed by the tissues, effectively prolonging its half-life. 3 to 5 hours after a meal, due to its
low affinity, the insulin – insulin antibody complex reaction shifts towards dissociation releasing large
amounts of biologically active insulin and triggering episodes of post prandial hypoglycemia. Several
treatments have been described including steroids, azathioprine, plasmapheresis and low carbohydrate
diets. Efficacy has been variable among case reports but all of them have shown a good correlation
between control of the underlying pathology, decrease in antibody titers and resolution of symptoms as
occurred in our patient.
[Date]
In conclusion insulin autoimmune syndrome (autoimmune hypoglycemia) whilst uncommon should be
part of the differential diagnosis of patients unexplained hypoglycemia. In particular the presence of an
insulin autoimmune syndrome should trigger a work up for paraproteinemias.
88
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Shudhanshu Alishetti, MD
Leukemoid Reaction in Extraintestinal Amebiasis
First Author: Shudhanshu Alishetti, MD Patrick Sarte, M.D., M.S., F.A.A.P., F.A.C.P.
Introduction: A leukemoid reaction is a leukocyte count greater than 50,000 cells/microL. Generally,
levels this high are related to a hematological malignancy or bacterial infections. This is a rare case
where extra-intestinal amebiasis presented as sepsis and a leukemoid reaction.
Case Description: A 65-year-old man of Mexican origin and no known past medical history presented to
the emergency room with confusion and general malaise. He had been complaining of left sided chest
pain and fatigue for three days prior to presentation. A chest x-ray in the ED was concerning for severe
pneumonia and patient was admitted to the ICU. A high-resolution chest CT was done at that point that
did not show any lung consolidations or pulmonary embolisms, but showed an apparent hepatic
abscess. An abdominal ultrasound confirmed the presence of 2 large hepatic abscesses. Antibiotics
were broadened to cover abdominal flora. The patient’s WBC count continued to rise, peaking at
57,700 cells/microL on day 5 of his hospitalization. Concurrently, his AST rose to 2355 and ALT rose to
575. One abscess was drained and yielded anchovy paste like material, consistent with an extraintestinal E. histolytica infection. 3 days later, the patient developed a rapidly growing R pleural
effusion, which was drained alongside the 2nd abscess. The 2nd abscess also drained anchovy paste like
material, while the effusion was found to be exudative. Once blood and fluid bacterial cultures returned
negative, antibiotic coverage was narrowed to Metronidazole. E. histolytica serum antibody was
positive. Patient improved significantly in his mentation, respiratory status, and hemodynamics during
his hospitalization, receiving a total of 3 weeks of Metronidazole and then transitioned to Iodoquinol
[Date]
Discussion: Invasive amebiasis occurs worldwide, most often in communities where fecal matter
contaminates drinking water. A host is infected by ingesting food with E. histolytica cysts. Excystation
occurs in the intestinal lumen and amoebic trophozoites invade the colonic mucosa, spreading
hematogenously to extra-intestinal locations, most commonly the liver. Abscesses are seen in <1% of
patients with E. histolytica infections. A mild to moderate leukocytosis and a positive E. histolytica
serum antibody are normally. However, in rare cases such as this one where the burden of disease is
high, a WBC count above 50,000 may be present. This may be misleading as it is more commonly seen
in pyogenic liver abscesses. Ameobic abscess material, though, classically appears anchovy paste
like. Treatment of such an infection is with nitroimidazoles. Drainage of abscesses is not required and
risks anaphylactic shock if abscess contents leak. However, drainage should be considered if there is
concern for abscess rupture or if patient is symptomatic.
89
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Mekhala Chandra, MD
Catecholamine Induced Peripartum Cardiomyopathy: A Rare Reversible Cause
Mekhala Chandra, MD1 Melissa E. Weinberg, MD2 Sara L. Swenson, MD, FACP1, California Pacific Medical Center
Department of Medicine1, CPMC Department of Endocrinology2, San Francisco , California.
Introduction: Catecholamine-induced cardiomyopathy is a rare but potentially life threatening
presentation of pheochromocytoma. Pre-transplant evaluation of patients with dilated cardiomyopathy
should include evaluation for pheochromocytoma.
Case: A 36 year-old G5A3P2 female was initially admitted to an outside hospital with acute onset of
chest pain and palpitations. In the emergency department, she became hypotensive and hypoxic and
was emergently intubated. An elevated beta-HCG led to the identification of an ectopic pregnancy,
which was medically terminated with methotrexate. A bedside echocardiogram revealed a biventricular
dilated cardiomyopathy (LVEF 25%). Her initial white blood cell count was 37.3 and troponin, 4.7. She
was managed emergently with an intraaortic balloon support and dobutamine and transferred to our
institution for possible heart transplant. Cardiac work-up included a normal coronary angiogram and
endomyocardial biopsy was negative. Abdominal ultrasound showed a possible left adrenal mass, which
was confirmed on abdominal CT as a 3.2 cm adrenal mass with peripheral enhancement. Twenty-four
hour urine metanephrines and catecholamines were elevated to 1483 mcg/24 hr and 125 mcg/24 hr,
respectively. We initiated phenoxybenzamine by gradually titrating upto 30 mg twice daily. Her
hemodynamic parameters subsequently improved. She underwent laparoscopic adrenalectomy, and
pathology was consistent with pheochromocytoma. Three months after her surgery, she remains
asymptomatic off all cardiac medications.
DISCUSSION: Pheochromocytoma should be considered in patients with unexplained heart failure.
Pheochromocytomas can present with cardiovascular complications in up to 19% of cases; apart from
hypertensive crisis, these most commonly include tachyarrhythmias (54%), myocardial infarction (32%),
and heart failure (18%). Cardiomyopathies can present with hypertrophic, dilated, or Takotsubo-type
physiologies. Catecholamines exert a direct toxic effect on myocardial cells causing myocardial edema
and myocardial and arterial wall fibrosis. Patients have undergone cardiac transplantation for presumed
idiopathic cardiomyopathy that was actually due to undiagnosed pheochromocytoma. Hence, it is
imperative to consider this diagnosis in patients with cardiomyopathy, especially if considering heart
transplant. Our patient illustrates that with appropriate treatment, cardiomyopathic changes are
reversible in over 90% of cases.
[Date]
Our patient lacked pheochromocytoma’s classic triad of episodic headache, tachycardia, and
diaphoresis. Her ectopic pregnancy likely triggered the unmasking of her pheochromocytoma with
fulminant heart failure. Pheochromocytoma in pregnancy is rare, and limited experience with diagnosis
and management among practitioners adds to its potential danger. However when considered, the
diagnosis is straightforward because pregnancy does not alter diagnostic levels of catecholamines or
metanephrines.Management with alpha and beta-adrenergic blockade prior to surgical resection
resembles that in non-pregnant women. However, optimal outcomes require an individualized approach
with collaboration among obstetricians, endocrinologists, cardiologists, and surgeons.
90
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Amy L Cummings, MD
Transplanted, pregnant and in pain: An imaging dilemma in a renal transplant
patient with urosepsis and continued pyuria
First Author: Amy L Cummings, MD Second Author: J Paul Finn, MD
Introduction: Pregnancy poses unique challenges in diagnosing and treating many common medical
conditions. Here we discuss the use of imaging in pregnancy and suggest ferumoxytol as an alternative
to gadolinium in contrast-enhanced magnetic resonance imaging (MRI).
Case Description: Our patient is a 21 year-old female G1P0 at 16 weeks with a congenital single
left kidney and end-stage renal disease from obstructive uropathy, since status-post deceased-donor
renal transplant at age 13 with stable graft function. Her pregnancy had been complicated by
recurrent urinary tract infections, and she had completed a third prescription of cephalexin one week
prior to presentation. Her immunosuppressive agents included azathioprine 75mg po daily,
prednisone 5mg daily and sirolimus 18mg po BID. Two days prior to admission, she noted insidious leftsided abdominal and back pain followed by fevers, nausea and vomiting. Her physical exam was
significant for tachycardia and exquisite left flank tenderness. Her WBC count was 13.4 with gross pyuria
on urinalysis; urine culture was positive for pansensitive Klebsiella pneumoniae. The patient was slow
to respond to treatment, and after 96 hours of intravenous cefazolin, she continued to complain
of exquisite left flank pain with continued pyuria on urinalysis. Ultrasound showed a viable intrauterine
pregnancy, unremarkable renal transplant and severe hydronephrosis of the native left kidney with
internal echoes. After extensive discussions with consulting services regarding the risks and benefits of
imaging as opposed to definitive surgical intervention, time-resolved contrast-enhanced 3D magnetic
resonance angiographic and venographic images of the abdominal and pelvic vasculature were obtained
using ferumoxytol. The patient received 510mg of ferumoxytol (iron equivalent 240 mg) without adverse
effect. These images showed no evidence of an inflammatory mass or abscess, and the suggestion of
renal enhancement of the native kidney supported continuing antibiotic therapy. Ultimately, after eight
days of treatment, the patient's symptoms began to resolve, and she was discharged on suppressive
antibiotics. Her graft maintained excellent function throughout her hospitalization, and her hemoglobin
level rose from 8.5 to 10.2 prior to discharge without additional hematopoietic measures. At 36 weeks,
the patient underwent pharmaceutical induction of labor for severe pre-eclampsia and delivered a
healthy 7 pound 12 ounce baby girl. Both mother and baby continue to do well and have met all
appropriate milestones.
[Date]
Discussion: Ferumoxytol, a superparamagnetic iron oxide agent, has been approved as an iron
replacement therapy for chronic kidney disease and more recently has been investigated as an
intravenous MRI contrast agent for those with compromised renal function. Its unique advantages
include an ability to delineate organ perfusion and vascularity at the time of injection and potentially
define inflammatory changes due to uptake by the reticuloendothelial system 24-48 hours after
injection. It may be used in those with glomerular filtration rates less than 30 and, because it does not
contain gadolinium and does not cross the placenta, its use in pregnancy is likely safer than gadolinium
based contrast agents with the added benefit of repleting iron in patients who may be deficient.
91
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Vidhi Doshi, MD
Malignant Solitary Fibrous Tumor of the Pleura
First Author: Vidhi Doshi, MD Second Author: Stephanie Zia, MD
INTRODUCTION: Solitary fibrous tumors are rare mesenchymal tumors originating from serosal surfaces.
Usually benign, they carry an excellent prognosis after surgical resection. We report an aggressive and
malignant case of this tumor that is not surgically resectable. Given the rare nature of the tumor, one
must recognize the signs and symptoms that can facilitate a prompt diagnosis. We also review the
pathologic features that suggest malignancy and describe treatment options when surgery is not
feasible.
CASE REPORT: A 55-year-old Caucasian woman with no significant past medical history presented with a
1-week history of acute onset worsening shortness of breath (SOB) with exertion and at rest. She denied
cough, fevers, chills, weight loss, or sick contacts. Physical examination revealed a confused, overweight
female in significant respiratory distress and hypoxic to 83% on room air. She had absent breath sounds
in the right lung field, with hearts sounds displaced to the left. The patient was intubated and
underwent bronchoscopy, thoracentesis with pleural fluid analysis, and CT guided biopsy, all of which
yielded non diagnostic results. She then underwent thoracotomy and biopsy, which revealed a
malignant solitary fibrous tumor. The tumor was deemed to be non-resectable, and the patient was
started on chemotherapy with temozolomide and bevacizumab. Currently, the patient is finishing her
first round of chemotherapy and is responding to treatment having had her tracheostomy tube removed
and with decreased SOB.
[Date]
DISCUSSION: Solitary fibrous tumors of the pleura are very rare tumors with an incidence of 2.8 per
100,000 individuals. Only 800 cases have been reported between 1931 and 2002. They are usually
benign in nature, but can be malignant and aggressive in 12-20% of cases. While working up a chest
mass, differentials can include lung carcinoma, germ cell tumor, sarcoma, thymic neoplasm, teratoma,
atelestasis, and neurogenic tumors. Unique to the tumor are paraneoplastic syndromes that may
present in some patients; symptoms include hypoglycemia or hypertrophic pulmonary
osteoarthropathy, none of which were seen in our patient. Malignant tumors have distinct pathology,
with areas of necrosis and or hemorrhage, high mitotic counts, cellular pleomorphism, and high
cellularity. Our patient’s tumor demonstrated necrosis and high cellularity. The mainstay of treatment is
complete resection, which is key to preventing recurrence and is the most important prognostic factor.
In cases in which surgery is not feasible, radiotherapy and/or chemotherapy may play a role in therapy.
Given the vascular nature of these tumors, they may respond to anti-VEGF combination therapy. The
regimen, consisting of bevacizumab and temozolomide or imatinib, may have some benefit in patients
with nonresectable disease. However, more research still needs to be done on developing a standard
treatment protocol.
92
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Masoud Ghaemmaghami
Pulsatile Venous Doppler Waveform of the Lower Extremities with Visible Swirling;
a Clue for Pulmonary Embolism
First Author: Masoud Ghaemmaghami
Introduction: We present a case of acute pulmonary embolism (PE) diagnosed by internal medicine (IM)
residents with bedside ultrasonography (US) when computed tomography angiogram (CTA) chest could
not be performed. Pulsatile venous doppler waveform of the lower extremities (LE) with visible swirling
was a clue to seek more enhanced bedside cardiac US to capture D-sign and McConnell’s sign which are
distinct cardiac ultrasonographic findings in acute PE.
Case: A 42 year-old male, otherwise healthy, presented with mid-sternal chest pain and worsening
dyspnea for one week. His vitals were BP 147/108, HR 110, RR 18, O2sat 97% on Room Air. Physical
exam showed no acute distress, no murmurs, and lungs were clear. Laboratory results were
unremarkable. Chest X-ray was normal. EKG showed sinus tachycardia with T-wave inversion in lead III
and V1-V4 which raised a suspicion for acute PE. However despite a detailed discussion, patient did not
consent for CTA chest which prompted the IM residents to perform bedside LE US to evaluate for deep
vein thrombosis (DVT). Pulsatile venous doppler waveform of the LE with visible swirling was noticed
without any evidence of DVT. This finding was a clue for elevated right sided pressure that lead to a
careful examination by bedside cardiac US which revealed D-sign and McConnell’s sign. The result of the
bedside US done by the IM residents strongly supported the suspected diagnosis of acute PE. Later, he
consented for CTA chest revealing large bilateral PE.
Discussion: Diagnosing acute PE can be challenging when CTA chest, the gold standard test, cannot be
performed. It is even more challenging in rural hospitals with limited ultrasonography service. Trained
IM residents on bedside US can make a difference for early detection and treatment of acute PE. D-sign
and McConnell’s sign are established US findings of acute PE. However, in our case, pulsatile venous
doppler waveform of the LE with visible swirling was detected as a clue for elevated right sided pressure.
Normally venous doppler waveform of LE is continuous with mild respiratory variation. To our
knowledge, there have been three studies that showed correlation between pulsatile doppler waveform
and elevated right sided pressure. All studies showed high specificity of > 85%.
[Date]
Conclusion: This case illustrates that bedside ultrasonography performed by trained residents can play a
major role in making the early diagnosis and treatment for acute PE. Although more studies are needed
to prove the relationship between pulsatile venous doppler waveform of the LE with visible swirling and
elevated right sided pressure, it can raise the suspicion for acute PE in the right clinical setting.
93
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Rola Khedraki, MD
An Atypical Road To Dialysis
Rola Khedraki, MD Zorawar Noor, MD James Rick, MD, PhD
Atypical hemolytic uremic syndrome (aHUS) is characterized by a continuous complement mediated
attack on vascular endothelial beds resulting in a thrombotic microangiopathy and multi-organ ischemia.
Failure of protein regulators to suppress the activity of the alternative complement cascade manifests as
thrombocytopenia, hemolysis, and uremia. Unlike typical HUS, which is triggered by Shiga-toxin, aHUS is
a primary disorder of complement regulation either secondary to genetic mutations or due to a trigger
event such as infection, pregnancy, or transplant.
A 59 year old male with history of HIV, well controlled on HAART therapy, presented to an outside
hospital with chief complaint of abdominal pain. There was no history of fever, illicit medications or
diarrhea. During his hospitalization, he developed pronounced expressive aphasia and lethargy but was
able to follow simple commands. A CT scan of the head revealed a left lacunar infarct and he was
transferred to our hospital for further care of a possible stroke. Shortly after arrival, he developed a
fever to 100.9 degrees Fahrenheit. Physical exam was remarkable for somnolence, disorientation, and
aphasia. Laboratory results demonstrated worsening thrombocytopenia, acute kidney injury, and
hemolysis (schistocytes, low haptoglobin, elevated LDH). Abdominal CT scan revealed terminal ileitis and
he was started on piperacillin-tazobactam. He was also empirically treated for presumed thrombotic
thrombocytopenic purpura (TTP) with plasmapharesis and methylprednisolone. However, this approach
was ineffective and he ultimately required hemodialysis. The addition of rituximab failed to improve his
condition, as he went on to develop seizure activity and evidence of further brain infarcts on imaging. A
normal ADAMTS13 activity level and negative Shiga-toxin assay led us to change our initial diagnosis of
TTP to aHUS likely triggered by his terminal ileitis. The diagnosis of aHUS was supported by a low
complement C3 level. Plasmapharesis was discontinued and treatment with eculizumab was initiated.
Two weeks later, his platelet count normalized, renal function improved, hemolysis resolved and he
regained full mental status. Seven weeks after initiating eculizumab, he no longer required dialysis.
[Date]
While TTP and aHUS share a common clinical presentation, their pathophysiology and management
differ. TTP is caused by a reduction in ADAMST 13 activity ( $600, 000 per year) has presented
worldwide ethical dilemmas regarding the need for continued therapy post renal and hematologic
recovery and criteria for discontinuation.
94
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Rachel J Klein, MD
Hepatocellular Carcinoma in a 25 year old man: Are steroids to blame?
First Author: Rachel J Klein, MD
Introduction: Long term use of androgenic-anabolic steroids (AAS) have been associated with liver
tumors. The majority of these tumors are benign while only a few reported cases in the literature are
malignant carcinomas as described in this case.
Case Presentation: Patient is a 25-year-old male with a 9 year history of anabolic and androgenic steroid
abuse who presented to the Emergency Department with a 2 month history of abdominal pain and
bloating, poor appetite and early satiety. He had lost approximately 35 pounds over the same
timeframe. Physical exam revealed a large tender mass palpable across the entire upper half of the
abdomen extending 6cm below the left and 4cm below the right costal margin. The remainder of his
exam was unrevealing though he did have an extremely muscular build.
Abdominal ultrasound revealed a large heterogeneous mass arising from the left liver. MRI performed
revealed a liver mass arising from the left lobe measuring 17.3 x 18.2 x 13.7cm with areas of
hemorrhage, scar and necrosis. Liver biopsy revealed well differentiated hepatocellular carcinoma
within the mass and normal parenchyma in surrounding liver without evidence of cirrhosis. Patient
underwent resection and declined adjuvant chemotherapy. He was subsequently seen in follow up with
resolution of abdominal pain, anorexia, and early satiety. He was followed by endocrinology to wean his
current exogenous testosterone usage. The patient subsequently moved abroad and was lost to followup.
[Date]
Discussion: This case highlights an atypical presentation of hepatocellular carcinoma. Though HCC is rare
outside of cirrhotics and Hepatitis B, it must be considered in any patient presenting with a liver mass
especially in the setting of exogenous anabolic and androgenic steroid abuse. This patient’s AAS abuse
likely contributed to his development of HCC given known risk of development of liver tumors with use
of androgens. This case highlights the importance of a good social history including medications received
without a doctor's prescription or recommendation. Screening for hepatic complications should be
considered for any patient using or abusing AAS.
95
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Chin C Lee, MD
Rare Valvular Aneurysms Secondary to Infective Endocarditis
Chin Lee, Parham Zarrini, Omeed Elboudwarej, Robert Siegel
Introduction: Infective endocarditis (IE) and the spread of infection to the surrounding tissue can result
in valvular aneurysms, paravalvular abscesses, and pseudoaneurysms. These rare complications can
occur subacutely even after completion of intravenous antibiotics. Consequently having routine
surveillance echocardiograms for patients with IE is important for the early detection and treatment of
these rare complications.
Case1:A 44-year-old man was admitted for group B streptococcal bacteremia. His initial transesophageal
echocardiogram (TEE) was normal with no evidence of valvular disease or vegetation. He was treated
with six weeks of intravenous ceftriaxone for presumed group B streptococcal IE with negative
surveillance blood cultures. After completion of antibiotic therapy a transthoracic echocardiogram (TTE)
showed new severe aortic regurgitation and aneurysmal enlargement of the right sinus of Valsalva
(SOV). A repeat TEE showed no valvular vegetations but demonstrated a pseudoaneurysm at the SOV
with the aortic valve right coronary cusp prolapsing into the pseudoaneurysm resulting in severe aortic
insufficiency. He underwent aortic valve repair and was found to have the pseudoaneurysm extending
into the commissural area with partial detachment of the left coronary cusp that were repaired with a
pericardial patch. The patient had an uneventful post-operative recovery.
Case2: A 20-year-old woman was admitted for group B streptococcal bacteremia. Her TTE showed a
vegetation on the anterior mitral valve leaflet (AMVL) and completed six-weeks of intravenous penicillin
with negative surveillance blood cultures. Two months later, a repeat TTE showed that the vegetation
was smaller in size but was now mobile and protruding into the left atrium. A followup TEE showed
complete resolution of the vegetation and minimal mitral regurgitation, but also the development of an
aneurysm of the AMVL. Six months later, she developed progressive dyspnea on exertion and
subsequent TEE showed ruptured chordae with severe mitral regurgitation and ballooning aneurysm of
the AMVL, without involvement of the aortic valve. She underwent urgent surgery, with resection of the
aneurysm, repair of the mitral valve and ruptured chordae, and reinforcement of the valve with an
anuloplasty ring. The patient had an uneventful recovery.
[Date]
Discussion: Valvular aneurysm and pseudoaneurysm are rare complications of IE. TEE is recommended
for early detection of IE because of its high sensitivity and specificity. Both of these cases demonstrate
the rare development of valvular aneurysms despite completing six weeks of intravenous antibiotics
with negative surveillance blood cultures. This illustrates the importance of surveillance
echocardiograms during the first year following completion of therapy. When valvular aneurysm is
detected, it is difficult to predict its risk of progression. However, symptomatic patients should be
evaluated for surgical correction.
96
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE John Brandon Lough, MD
Acute Cholangitis Secondary to Hepatic Hydatid Cyst Disease with Cyst SuperInfection
First Author: John Brandon Lough, MD Sarbjit Sandhu, MD Tanaya Bhowmick, MD
Introduction: Echinococcosis, or Hydatid disease (HD), is an infection caused by taeniid cestodes belonging
to the genus Echinococcus. The following is a reporting of the management of a case of acute cholangitis
secondary to hepatic hydatid cyst disease resulting in cyst super-infection.
Case: A 24-year-old male with no significant past medical history presented to the emergency department
with a one week history of progressively worsening right upper quadrant (RUQ) discomfort, skin yellowing,
and fevers to 102. Physical exam was notable for jaundice, scleral icterus, and tender hepatomegaly palpable
to 4 cm below the costophrenic angle. Labs were significant for a leukocytosis to 17.4 (x103 cells/mm3), AST
390 (units/L), ALT 557 (units/L), Alk phos 504 (units/L), T bili (mg/dL) 8.7 with D bili 6.3 (mg/dL). Computed
tomography (CT) imaging of the abdomen showed two large cystic lesions within the left lobe of the liver that
measured 7.7cm x 7.7cm and 5.2cm x 4.7cm, with the common bile duct running adjacent to the masses with
secondary involvement. RUQ ultrasound showed a complex cystic mass located in the left lobe of the liver,
another mass deep to the right lobe, and a dilated common bile duct to 14mm.
Given the obstructive cholestasis picture and concern for hepatobiliary infection, the patient was started on
piperacillin-tazobactam and taken for endoscopic retrograde cholangiopancreatography (ERCP). Biliary
stenting with sphincterotomy was performed which returned a gelatinous substance, as well as purulent
drainage. Albendazole was started empirically given the ultrasound findings of the masses being complex
and cystic, suggesting hydatid cyst disease. Broad-spectrum antibiotics were continued given the biliary
drainage character and concern for super-infection of the cysts. Echinococcus Ab returned positive during the
admission, confirming the diagnosis. Given the size of the cysts with extensive liver involvement, complete
resection was not a feasible option. As the patient’s labs and clinical course improved with medical
management, the patient was continued on albendazole and broad-spectrum antibiotics with planned
reevaluation following a two-month course of antimicrobials.
Discussion: Management of uncomplicated cysts is primarily surgical resection with adjuvant use of an
anthelmintic agent (eg, Albendazole, mebendazole). Percutaneous aspiration has historically been
discouraged due to the risk of anaphylactic shock. Preoperative treatment with albendazole for 1-3 months
is an option and has shown to reduce the number of viable cysts found on surgery. Percutaneous aspiration,
injection, and re-aspiration (PAIR), where the cyst(s) is drained with a fine needle or catheter, followed by
instillation of a protoscolicidal substance (eg, hypertonic saline or absolute alcohol) and reaspirated, has
emerged as a potential first line treatment. Optimal treatment approach remains unclear, as there have
been no clinical trials comparing all treatment modalities together.
[Date]
The patient was not a candidate for resection given the extent of the disease, and was not a candidate for
PAIR due to biliary involvement- a World Health Organization contraindication. Therefore, the most
appropriate approach was to decrease the size of the cysts with medical management with the intention of
complete resection of the cysts at a later date.
97
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Mehvish Mahmood, MD
The Great Mimicker- Melioidosis
First Author: Mehvish Mahmood, MD, Dr. Mandeep Singh, MD,
Introduction: Many US veterans returning from Vietnam War who presented with fever and other
various symptoms were diagnosed with Melioidosis. Inhalation of contaminated dust raised from
helicopter rotor blades in Vietnam was the possible source of inoculation. Although endemic in South
East Asia and Northern Australia, melioidosis is rare in the USA. On average 0-5 cases are diagnosed
annually. Therefore, a high suspicion in recent travelers to endemic areas and well-timed diagnosis is
pivotal in preventing fatality.
Case Description: 60 year old Filipino male with past medical history of poorly controlled Diabetes
Mellitus (HbA1c:12%), Hypertension and Dyslipidemia, was seen in medicine clinic three weeks after
returning from Philippines. He complained of episodic fever, up to 101 degrees Fahrenheit and 17
pounds weight loss during past three weeks. While in Philippines, he also had an ear infection after
swimming in fresh water, which was treated with oral amoxicillin with complete resolution. Primary
workup during his clinic visit was significant for leukocytosis of 14,100 per microliter and positive blood
cultures for Gram-negative rods. Despite treatment with two days of Ceftriaxone (intramuscular) and
Ciprofloxacin (oral), patient remained febrile and was admitted to hospital for intravenous antibiotics
and better glycemic control. Final blood cultures grew Burkholderia pseudomallei. Chest x-ray, HIV, and
Urine culture were negative. Based on culture sensitivities, he was started on TrimethoprimSulfamethoxazole and Ceftazidime. Subsequently, leukocyte count normalized, patient remained
afebrile and was discharged home after two days of hospitalization. He completed six weeks of oral
Trimethoprim-Sulfamethoxazole and four weeks of continuous intravenous Ceftazidime with complete
resolution of symptoms.
[Date]
Discussion: Melioidosis is caused by bacterium Burkholderia pseudomallei. At risk are individuals with
chronically immunosuppressed states such as, poorly controlled diabetes mellitus, alcoholism and
chronic renal or liver disease. Typically seen in South East Asian countries, it is now an emerging
infection in India, Africa, and Middle East. Contaminated soil or water exposure by contact, ingestion or
inhalation causes infection. The spectrum of clinical manifestations may vary from a localized infection
to raging widespread bacteremia. Though the most common presentation is pneumonia with symptoms
similar to pulmonary tuberculosis, it can also present as encephalomyelitis, septic arthritis,
osteomyelitis, skin and visceral organ abscesses, involving renal, splenic, prostatic and hepatic sites,
hence making this disease a great mimicker. Therefore, vigilance in the suspicion of rare diseases like
melioidosis, especially in travelers to endemic areas and obtaining targeted labs such as blood cultures
are crucial in preventing adverse outcomes.
98
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Stephanie Mai, MD
Bedside Lung Ultrasound in the Diagnosis and Management of Pneumonia in the
ICU Setting
First Author: Stephanie Mai, MD Second Authors: Emily Barrett, MD Vi Am Dinh, MD
Introduction: Lung ultrasound (LUS) has been increasingly used as an effective tool in the assessment of
pulmonary parenchyma of critically ill patients. It has reported to have high sensitivity and specificity in
aiding in the diagnosis of pulmonary edema, effusion, infarcts, pneumonia, and interstitial lung disease.
Advantages of LUS in critically ill patients include portable bedside assessment, real-time data
acquisition and analysis, timely serial examinations without utilization of radiation and also the ability to
guide management. We present a case where findings on LUS were used in conjunction with traditional
chest x-rays (CXR) to aid in diagnosis and management of pulmonary-interstitial syndrome.
Case: A 27-year-old male with a history of widely metastatic mucoepidermoid carcinoma presented to
the Emergency Department (ED) for acute on chronic worsening dyspnea and was admitted to the
Medical Intensive Care Unit (MICU) for acute respiratory distress. The patient was on low-flow oxygen
via nasal cannula at home but had increasing oxygen demand over the previous 2 days requiring 15 liters
on non-rebreather mask in the ED. Initial single view CXR demonstrated a large right pleural effusion.
Following chest tube placement 2000ml of sero-sanguinous fluid was expressed. Subsequent CXR
showed resolution of the pleural effusion and non-specific parenchymal findings.
The day after CXR showed an opacificaton of the right lung field which was read as reaccumulating
pleural effusion. However, bedside LUS revealed hepatization and air bronchograms in the right middle
lobe consistent with a right middle lobe pneumonia and a small pleural effusion. Based on the LUS and
clinical exam, a diagnosis of combined pneumonia and pleural effusion was made and the patient was
placed on antibiotics. During his admission, the patient became unable to tolerate supine positioning for
imaging modalities such as CT due to his dyspnea and painful spinal metastases. Serial LUS studies
demonstrated progressive resolution of B lines, and presence of prominent A lines, suggesting
resolution of the underlying pneumonia.
[Date]
Conclusion: While the application of ultrasound for initial evaluation of thoracic trauma is wellestablished, the employment of LUS to resolve non-traumatic diagnostic ambiguity on CXR and serial
pulmonary exams to guide management in critically ill patients is recent. Prior studies have shown LUS
has an excellent sensitivity and specificity comparable to two-view CXRs in diagnosing pneumonia. We
demonstrate the utilization of LUS in evaluating lung parenchyma and in guiding our management for a
patient with acute dyspnea found to have pleural effusion and pneumonia. CXR results alone may have
delayed treatment of the underlying pneumonia. LUS is inexpensive, easily accessible and may assist in
the diagnosis and management of critically ill patients with mixed or ambiguous findings on CXR.
Additionally, LUS provides timely imaging and can assist in tracking responses to therapy.
99
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Nareg Minaskeian, MD
Pre-workout Caffeine Supplement Induced Cardiac Arrhythmia Leading to Brain
Death
First Author: Nareg Minaskeian, MD Additional Authors: Nikhil Shah, MD., Mark Bradburne, MD.
Introduction: Many young adults who exercise nowadays drink pre-workout supplements, most of
which contain excessive amounts of caffeine, to augment their work-out regimen. These pre-workout
supplements are not FDA approved, nor have there been any studies investigating the toxic effects of
such supplements coupled with exercise. Caffeine, a methylxanthine, acutely causes a rise in
(nor)epinephrine concentrations, blood pressure, systemic vascular resistance, and arterial
stiffness. Although the median lethal dose of caffeine for humans is estimated to be about ten to
fourteen grams, we present a case of acute arrhythmia leading to anoxic brain injury and death at a
significantly lower dose.
Case Presentation: A previously healthy 24-year-old male was brought in by ambulance to the
emergency department after being found down and unresponsive at the gym. Prior to arrival he was
defibrillated and intubated. He was defibrillated again for ventricular fibrillation in the emergency
department and transferred to the intensive care unit. Labs returned with markedly elevated cardiac
enzymes, leukocytosis and an elevated creatinine. A urine drug screen was negative. Physical exam
revealed a fit young adult with an unremarkable cardiac, pulmonary and abdominal exam. Neurologic
exam revealed a Glasgow Coma Scale score of 2 [E1V(T)M1] but intact pupillary, gag, cough and corneal
reflexes. Vital signs were within normal limits. A CT scan of the head showed mild diffuse cerebral
edema and an echocardiogram was demonstrative of global hypokinesis with an ejection fraction of
about 40%. A history taken from family revealed that the patient took a pre-workout supplement, Mr.
Hyde, prior to exercising. According to the nutritional facts, one serving contains 419mg of
caffeine. Throughout admission, the patient remained intubated and comatose with no changes in
neurologic exam. However, on day four of admission, the patient's pupils became fixed and dilated, and
he lost his gag, cough and corneal reflex. Repeat CT scan of the head now showed severe worsening of
the cerebral edema without herniation. After a family discussion, care was withdrawn and the patient
expired on day six of admission.
[Date]
Discussion: The toxic effect of caffeine has been widely studied, though there has not been any
research on the toxicity of pre-workout caffeine supplements. We conclude that an excessive amount
of concentrated caffeine, coupled with a highly adrenergic response from intense exercise caused a
significant diffuse coronary artery vasospasm in our patient that led to arrhythmia, severe anoxic brain
injury and clinical brain death. Our case highlights the dangers involved with taking pre-workout
supplements with caffeine, even at fractions of the median lethal dose, and the need for possible
regulation of such substances.
100
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Sophia Mytrang Nguyen, MD
Wilson Disease Disguised as Drug Induced Liver Injury from Nitrofurantoin
Sophia Mytrang Nguyen, Katelyn Gamson, Richard Garcia-Kennedy, Edward Holt
A 26 year-old Latina presented with one month of progressive fatigue, abdominal pain, and bilious
emesis. She reported minimal alcohol intake, no use of complementary medicines, no new sexual
partners and no intravenous drug use. She had recently completed a course of nitrofurantoin for acute
cystitis. Physical exam revealed a moderately obese, jaundiced woman with scleral icterus. Her
abdomen was non-distended with a soft liver edge, but was diffusely tender to palpation.
She had bilateral lower extremity edema and palmar erythema. There was no asterixis. Initial laboratory
work up included the following: WBC 19.9K/uL, hemoglobin 8.6g/dL, platelets 195K/uL, INR 2.8, albumin
1.3g/dL, total bilirubin 7.6mg/dL, indirect bilirubin 1.9mg/dL, ALT 82U/L, AST 129U/L, alkaline
phosphatase 66U/L, iron 56ug/dL, transferrin saturation 45%, ferritin 1170ng/mL, 17.5% reticulocytes,
haptoglobin 53mg/dL, LDH 294U/L, and a negative direct Coombs test. The G6PD, alpha-1-antitrypsin,
ceruloplasmin and acetaminophen levels were normal. Serologic markers for autoimmune,
inflammatory, and infectious hepatitis were negative.
Abdominal CT showed a patent hepatic portal venous system. Liver biopsy revealed minimal
inflammation with a background of moderate patchy microvesicular steatosis and lobular collapse
without regenerative nodules. Given the presence of hemolytic anemia with a normal haptoglobin and
extensive hepatocellular injury in the context of recent antibiotic exposure, drug-induced liver injury
from nitrofurantoin was suspected. During her hospitalization, she became more encephalopathic and
developed worsening renal function, hyperbilirubinemia, and coagulopathy. Further work-up revealed
24-hour urine copper was elevated at 159mcg and repeat ceruloplasmin was 13.8mg/dL (normal 2060mg/dL). An ophthalmic exam revealed Kayser-Fleisher rings. Liver biopsy showed a quantitative
copper level of 752mcg/g dry-weight (normal <250mcg/g). She exhibited heterozygosity for the ATP7B
mutation.
[Date]
A diagnosis of fulminant hepatic failure secondary to Wilson disease was made. She underwent
orthotopic liver transplantation 3 days later, and recovered well following surgery. Wilson disease (WD)
is an autosomal recessive disorder of impaired copper excretion leading to multi-organ damage. WD is
typically recognized by the presence of Kayser-Fleischer rings, neurologic symptoms, and a low serum
ceruloplasmin level. However, the diagnosis of WD in the setting of ALF is challenging given the poor
diagnostic performance of various measures of copper metabolism. In particular, reduced serum
ceruloplasmin can be less reliable and specific in this setting. Diagnostic clues for WD in ALF include:
female predominance, presentation before age 40, hemolytic anemia and a sub-normal serum alkaline
phosphatase. Nitrofurantoin is a commonly prescribed oral antibiotic that can cause ALF weeks
following intake and can surprisingly uncover underlying Wilson disease. Reevaluating our initial
diagnosis of hepatic toxicity from nitrofurantoin and considering the diagnosis of WD proved to be an
essential diagnostic step in this case.
101
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Quan M Nhu, MD, PhD
Breathless before the (Scorpion) King: Acute eosinophilic pneumonia following
scorpion envenomation
First Author: Quan M Nhu, MD, PhD Carrie D. Chun, MD
Introduction: Scorpion envenomation can cause both local and systemic manifestations. While most
cases are minor, scorpion envenomation can cause pulmonary edema, myocardial depression,
hypotension, and multi-organ failure. We report herein a case of acute eosinophilic pneumonia
presenting as acute hypoxemic respiratory failure following scorpion envenomation.
Case Description: A 41-year-old male with a two-week exposure to Bactrim for a recent onset of bursitis
presented with worsening dyspnea 4 days after envenomation by a bark scorpion (Centruroides
sculpturatus). Upon arrival, he had T 37.3 ºC, BP 122/65, HR 91, and RR 18. He initially had an oxygen
saturation of 95% on room air; however, within 2 hours of arrival, he quickly desaturated to
88%. Physical exam demonstrated bilateral lung crackles. There was no swelling, erythema, or streaking
in the vicinity of the scorpion sting. CBC, BMP, lipase, CK, CK-MB, and BNP were within normal
limits. Chest CT showed extensive patchy infiltrates and was negative for pulmonary
embolus. Transthoracic echocardiographic examination showed normal LVEF of 58.7%, without
evidence of wall motion abnormalities or right ventricular dilation or strain. The patient was transferred
to the ICU on hospital day two for acute hypoxemic respiratory failure. The patient was intubated and
placed on lung protective ventilation per ARDSNet protocol. Extensive evaluation for infectious,
vasculitic, and rheumatologic causes of respiratory failure, including a bronchoalveolar lavage, was all
non-diagnostic. Video-assisted thorascopic surgery (VATS)-mediated lung biopsy demonstrated an acute
eosinophilic pneumonia superimposed on subacute reparative changes, temporally consistent with lung
injury associated with scorpion envenomation. The patient was treated successfully with systemic
corticosteroids and discharged home on supplemental oxygen and a prolonged corticosteroid course.
[Date]
Discussion: Bactrim is known to cause acute lung injury (ALI). However, ALI in the setting of scorpion
envenomation is an under-recognized clinical presentation. To our knowledge, this is the first report of
acute eosinophilic pneumonia associated with scorpion envenomation. Amaral et al. reported acute
lung injury and increased alveolocapillary membrane permeability in scorpion sting, resulting in
pulmonary edema and death of a 16-year-old boy with microscopic features of ARDS (Toxicon
1994). D’Suze proposed the term Scorpion Venom Respiratory Distress Syndrome using a rabbit model
of envenomation-induced lung injury (Toxicon 1999). Coelho et al. showed that scorpion venom can
drive chemokine production, neutrophil influx and edema formation in murine lungs (Toxicon 2007). In
support of our observation, Shah et al. reported the association between pulmonary infiltrates with
eosinophilia (PIE) syndrome and scorpion sting in a young adult male (Chest 1989). Taken together,
scorpion venom has the capacity to induce direct and indirect lung damage and thus, can potentially
contribute to the development of respiratory distress and failure. Scorpion envenomation, combined
with Bactrim, likely contributed to the rapid clinical deterioration in this young patient on presentation.
102
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Jane Park, MD
Road Tripper Arrives at a Road Block: Managing Acute Submassive Pulmonary
Emboli with Thrombolytic Therapy
First Author: Jane Park, MD Second Author: Yfa Sparks, MD Last Author: Maggie So, MD
Acute pulmonary embolism is a common, often fatal event. While thrombolysis is indicated with
massive PE, management of submassive PE with fibrinolytics is under debate. Here we present a case of
submassive PE managed with ultrasound-enhanced, catheter-directed tPA. A 68-year-old gentleman
with urinary retention presented with recurrent syncope. The patient had embarked on a crosscountry road trip and made pit-stops for intermittent foley catheterization, despite starting silodosin
and tamsulosin. When he reached the Bay Area, he complained of “chest congestion,” left leg swelling,
and episodes of slumping over unconscious.
Physical exam was notable for orthostatic hypotension, tachycardia, no murmurs, no elevated JVP, and
enlarged left lower extremity. Initial labs revealed troponin elevation to 1.4, BUN 27, and creatinine of
2.16. Lower extremity Doppler showed acute left lower extremity deep vein thrombosis and CTA
demonstrated bilateral pulmonary emboli with possible lower lobe hemorrhage. Bedside
echocardiogram showed severe right ventricular systolic dysfunction, severely enlarged right atrium,
large right atrial thrombus (about 2cm), and severe pulmonary hypertension. CT of the abdomen/pelvis
revealed a bulky, lobular prostate highly concerning for prostate cancer.
The patient’s hypercoagulable state from his underlying prostate cancer along with the hemostasis
during his road trip was a recipe for Virchow’s triad. While ultimately important to treat his underlying
malignancy, there was a critical need to address our patient’s high-risk mortality in the acute setting. RA
thrombus with acute PE is associated with higher mortality and risk of hemodynamic compromise. RV
dysfunction is associated with a twofold increase in PE-related mortality. EKOS catheter is an FDAapproved treatment of PE and the ULTIMA trial showed improved outcomes with reversing RV dilatation
at 24hrs, when compared to heparin anticoagulation alone. However risks include bradycardia, heart
block, as well as hemorrhage. Risk stratification for our patient was high so we pursued therapy that
might result in early hemodynamic improvement with EKOS. This is a rare case when submassive
pulmonary emboli could illustrate the utility of ultrasound-enhanced, tPa-directed therapy in critically ill
patients.
[Date]
Cardiothoracic Surgery, Interventional Radiology, and Vascular Surgery were consulted to address the
submassive PE. While the patient was hemodynamically stable, the evidence of severe right ventricular
dysfunction, extensive clot burden, and the right atrial thrombus signaled a high-risk situation. Thus, the
decision was made to place the EkoSonic (EKOS) catheter in the pulmonary artery for ultrasoundenhanced and tPA-directed thrombolysis, rather than thrombus extraction or traditional systemic
heparin anticoagulation. Subsequent evaluation showed that the pulmonary artery clot diminished, the
RA thrombus dissolved, with interval improvement in RV function, and the patient was transitioned to
systemic heparin therapy. Ultimately, his hospital course was complicated by cardiogenic shock,
requiring pressors, intubation, and dialysis. Fortunately he improved and was successfully extubated and
prostate cancer treatment was initiated.
103
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Nicolas D Prionas, MD, PhD
Carbapenem Neurotoxicity: A Case Report
Nicolas D Prionas MD, PhD
With the increasing prevalence of antibiotic-resistant organisms, Carbapenem use is widespread and
relatively well tolerated. This case illustrates a very rare side effect of Ertapenem-induced neurotoxicity,
the symptoms of which can be misleading.
Three months prior to case presentation, a 59 year old woman with a history of methamphetamine
abuse and intravenous drug use presented septic with Methicillin-sensitive Staphylococcus Aureus
(MSSA) bacteremia. MRI studies suggested right medial clavicular osteomyelitis, thoracic osteomyelitis
(T4-T5), thoracic pre-vertebral abscesses (T4-T6), and spinal leptomeningeal enhancement. Her
abscesses were drained and cultures were positive for MSSA. She was treated with broad spectrum
antibiotics and discharged to a skilled nursing facility (SNF) with 6-8 weeks of IV Nafcillin. An SSRI was
started for depression. The patient presented 2 weeks later with abdominal pain, nausea, vomiting,
and urinary retention. Repeat MR imaging of the spine showed a lumbar anterior epidural abscess (T11L2) and mild stenosis at T4-T5 in the presence of previously described abscesses. She underwent
thoracic decompression laminectomy, partial facetectomy, partial T4 corpectomy, instrumented fusion
of T4-T6, and non-instrumented fusion at C7. Blood cultures grew Lactobacillus, so antibiotic coverage
was broadened to Ertapenem and Rifampin due to spinal hardware.
Two weeks later, the patient presented with altered mental status (AMS), agitation, and acute kidney
injury (AKI) (serum creatinine 1.5 mg/dL, baseline 0.5-0.8 mg/dL). She had pressured rambling speech
and was only oriented to self and place. She was tremulous and hyper-reflexic and required redirection,
intermittent use of restraints and antipsychotic medications. Initially, there was concern for serotonin
syndrome given recent initiation of an SSRI; however, she previously tolerated the SSRI well and did not
improve with discontinuation. Ertapenem was changed to Meropenem for Pseudomonal coverage. The
patient’s AKI improved after fluid rehydration with normal creatinine by hospital day 3. On hospital day
5, Carbapenems were discontinued out of concern for neurotoxicity. Cefazolin was started. The patient’s
mental status dramatically improved by hospital day 6 with more coherent and linear speech and
orientation to person, place, and situation. Over the next 5 days, she had waxing and waning agitation
with minor delusions which improved with sleep hygiene, thiamine, and minimal antipsychotics. At
discharge, the patient’s mental status was at baseline and she was transferred to SNF on Doxycycline
(Lactobacillus coverage), Rifampin, and Nafcillin.
[Date]
Ertapenem neurotoxicity, although rare, has been observed in patients with ESRD with poor dialysis
compliance or with inappropriate dosing. It has rarely been seen in AKI. This case demonstrates the rare
risk for Carbapenem neurotoxicity, especially in the elderly with AKI. The sudden decrease in GFR likely
caused Ertapenem levels to suddenly increase inducing neurotoxicity. In the setting of persistent AMS
while on Carbapenem antibiotics, neurotoxicity should be considered and alternative antibiotics
administered when possible.
104
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Kristin E Schwab, MD
When Typical Provokes the Atypical: CMV Triggering an Unusual Presentation of
Atypical Mycobacterium
Kristin Schwab, MD; Patrick Ahearn, MD; Edward Ha, MD
Although cytomegalovirus (CMV) and mycobacterium represent two of the most common infectious
pathogens affecting transplant patients, general internists must be aware of the subtle and synergistic
ways in which these pathogens can present in immunocompromised patients.
A 43-year-old male with end stage renal disease secondary to IgA nephropathy presented six years post
renal transplant with five days of acute-on-chronic diarrhea. He had been suffering from one year of
intermittent diarrhea with an associated 30 pound weight loss. In the emergency department, he was
afebrile and hemodynamically stable with a normal abdominal examination. Stool was negative for
bacteria, viruses, acid fast bacilli, and ova and parasites. He underwent a colonoscopy on hospital day
four that revealed multiple red punched-out ulcers in the terminal ileum. Immunohistochemistry
revealed CMV-positive cells. Given this, he was started on IV ganciclovir for CMV enteritis and had
resolution of his diarrhea. On hospital day 10, he developed fevers to 39.2 ºC and night sweats. A
computed tomography (CT) scan of the chest showed the new development of extensive perilymphatic
nodules and prominent peribronchial thickening when compared with a CT scan from admission. A
pulmonary biopsy specimen revealed multiple bronchial wall granulomas with positive acid fast bacillus
(AFB) staining. Of note, four sputum AFB samples had been previously collected and found to be
negative for mycobacterium. Ultimately, blood AFB cultures taken at the time of admission grew out
mycobacterium avium complex (MAI).
He has since completed greater than six months of triple-antibiotic therapy for MAI with ethambutol,
azithromycin, and a fluoroquinolone. A CT chest scan obtained three months post treatment initiation
showed persistent mediastinal lymphadenopathy but improved peribronchial and interstitial disease
with only minimal scarring. He has gained greater than 20 pounds and has remained disease-free
without fevers, chills, cough, shortness of breath, or diarrhea. This case illustrates the unique
manifestations of common infectious pathogens in immunosuppressed patients. Mycobacterial disease
classically presents with slow and progressive symptoms, with MAI-infected patients often presenting
after greater than thirty days of symptoms. Our patient’s abrupt clinical and radiographic presentation
suggests a new perspective on pulmonary mycobacterial disease. In addition, our case suggests that
acid-fast bacillus infections need to be strongly considered in immunocompromised hosts with
pulmonary nodules even in the setting of negative AFB sputum cultures.
[Date]
To our knowledge, only one other case of CMV gastrointestinal disease followed by pulmonary
mycobacterial infection exists. In both of these cases, pulmonary mycobacterial disease began only after
the initiation of ganciclovir for CMV enteritis. Therefore, our case also suggests that in the setting of
CMV disease, immunomodulation from the virus or the antiviral medication can lead to recrudescence
of other infectious diseases.
105
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Sarthi R Shah, MD
Battling Influenza: Extra-Corporeal Membrane Oxygenation and an Emerging Role
in Influenza Associated Acute Lung Injury.
First Author: Sarthi R Shah, MD Second Author: Ragheb Assaly, MD
Introduction: The cumulative rate of hospitalization due to influenza, across all age groups, was 35.6 per
100,000 between October 2013 and April 2014. Among these cases of hospitalized patients there is an
increased mortality rate in those presenting with superimposed bronchopneumonia, as well as those
who develop acute respiratory distress syndrome (ARDS). We report one such case in which an initially
false negative rapid influenza test potentially delayed appropriate therapy, and where extracorporeal
membrane oxygenation was successfully used to treat our patient.
Case report: A 52 year-old female was transferred to our institution in vent-dependent respiratory
failure. She was initially found unresponsive at home. Patient’s family was able to provide a history
stating that she had been complaining of muscle aches, nausea and weakness prior to admission. She
had not had any shortness of breath prior to arrival at the outlying institution. While there, she had
rapid decline in respiratory function and was intubated. Rapid influenza swab done at the previous
institution was negative.
On arrival to our institution, a chest x-ray showed diffuse bilateral infiltrates. Initial arterial blood gas on
arrival to our institution showed a pH of 7.19, a PCO2 of 55 mm Hg, P02 of 68 mm Hg and HCO3 of 21
mmol/L while being mechanically ventilated in assisted-control mode at a rate of 14 breaths per minute
with an FI02 of 100%, and a tidal volume of 600 cc. The patient was evaluated by the intensive care team
as well as the cardiothoracic surgery and diagnosis of ARDS was made along with a decision to utilize
ECMO. Rapid influenza swab at the previous facility had been negative, but due to the presentation and
recent flu-like symptoms, ostelamvir was initiated along with broad-spectrum antibiotics. A
bronchoscopy was performed emergently to obtain bronchial washings for definitive diagnosis. Patient
was found to have influenza A with superimposed staphylococcus auerus. With continued antibiotic
therapy and ECMO support, patient eventually recovered and was weaned from ECMO. Through a
steady recovery over the course of 5 weeks, the patient was fully weaned from ECMO, mechanical
ventilation, and was eventually discharged.
[Date]
Conclusion: It remains important for clinicians to be aware that a rapid influenza test does not rule out
influenza in those patients where influenza can be suspected. In patient’s presenting with ARDS and
Influenza, the ECMO has an emerging role as a treatment, however retrospective studies do not show
clear efficacy. Although several retrospective studies utilizing ECMO in influenza patients exist, few have
shown a clear decrease in morality or hospital length of stay.
106
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Gautam J Shah, MD
Vasculitic Neuropathy as Initial Presentation of Granulomatosis with Polyangitis
(GPA)
Gautam Shah MD, Ana Nunes MD, Khamisah M. Barger MD, Tanya-Sue Winey MD
A previously healthy 66 year-old male was evaluated for pain and numbness of the bilateral plantar
surfaces which started two days into a cross-country road trip. This progressed over one week into
severe bilateral leg pain which left him unable to walk. Over the next four weeks, he experienced
intermittent bilateral lower extremity edema which improved with furosemide. One week prior to
presentation, he endorsed burning pain and numbness in his arms. He also reported a twenty five pound
weight loss over six months, fatigue, and recent onset of jaw pain while eating. He presented for
evaluation five weeks after the initial onset of his symptoms. At presentation, vital signs were within
normal limits, and the physical examination was notable for mild lower extremity edema, 3/5 left arm
abduction/extension strength, 3/5 hip flexion strength bilaterally, and 0/5 lower extremity strength
distal to the knees bilaterally with impaired vibration/proprioception/pinprick sensation. Bilateral
brachioradialis reflexes were intact; bilateral patellar and Achilles reflexes were absent.
Laboratory testing revealed elevated ESR, CRP, troponins, and CKMB. Lumbar puncture was within
normal limits; brain MRI showed areas of ischemic infarct in the right cerebral hemisphere; and EMG
demonstrated decreased amplitude in the bilateral upper and lower extremities as well as prolonged
distal latency and slow nerve conduction velocity in the upper extremities. Additional diagnostic
laboratories revealed positive c-ANCA and proteinase 3 (PR3) antibodies with negative HBV, HCV, and
HIV; this was suggestive of GPA. Confirmatory testing with sural nerve biopsy demonstrated lymphocytic
infiltration consistent with a vasculitic neuropathy. He was also felt to have cardiac involvement with his
vasculitis, based on his elevated cardiac markers. Echocardiogram revealed septal wall hypokinesis with
a normal angiogram. He was started on high-dose steroid therapy as well as induction therapy with
rituximab, and was eventually transitioned to oral prednisone. At an outpatient clinic visit two weeks
after discharge, his upper extremity strength and lower extremity sensation had improved, although he
still had bilateral foot drop.
Antineutrophil cytoplasmic antibody (ANCA) associated vasculitides include granulomatosis with
polyangitis (GPA), the Churg-Strauss syndrome, microscopic polyangitis, and pauci-immune
glomerulonephritis. GPA leads to vasculitis and granulomatosis of small to medium-sized blood vessels
and initial presentation typically involves ear-nose-throat complaints (90%) or respiratory complaints
(75%). Less frequently does it present with primarily peripheral nerve impairment (20%)*. Although
vasculitides were not high on our initial differential diagnosis, the negative lumbar puncture results and
overall constellation of symptoms forced the team to broaden our differential. This interesting case
serves as a reminder to always consider vasculitis in the differential diagnosis of a patient presenting
with weakness.
[Date]
References: *Berden A, Göçeroglu A, Jayne D, et al. Diagnosis and management of ANCA associated
vasculitis. BMJ. 2012 Jan 16;344:e26.
107
CALIFORNIA POSTER FINALIST - CLINICAL VIGNETTE Bryant W Wilson, MD
Testicular Tuberculosis: A Rare Presentation of Extra-Pulmonary TB
First Author: Bryant W Wilson, MD
A 43 year old Hispanic male presented with a one month history of testicular pain with draining purulent
lesions unresponsive to antibiotics. Further history revealed that he also had two weeks of a productive
cough and ten pound weight loss.
CT chest showed a miliary pattern of nodular infiltrates throughout both lungs with cavitation. CT
abdomen illustrated bilateral hydronephrosis with an infiltrative process involving the right renal
collecting system and ureter, and a heterogeneous mass involving the left testicle. Sputum, urine and
scrotal wound samples were all 4+AFB positive and cultures grew Mycobacterium tuberculosis.
Subsequent Quantiferon gold was positive.
The patient required bilateral nephrostomy tubes for his hydronephrosis and extensive ureteral
involvement. Standard anti-tuberculosis treatment was initiated, but had to be revised due to
phenotypic drug resistance to isoniazid, pyrazinamide and streptomycin. His course was complicated by
repeat episodes of urosepsis, although on follow up his left testicle has remained viable.
Genitourinary tuberculosis occurs in about 20% of extra-pulmonary disease, with the most common site
being the kidney, and then the ureter, epididymis and testicle in descending order.
Dissemination of Mycobacterium tuberculosis bacilli after infection results in subsequent involvement of
various organs. Testicular involvement is often a result of retrograde extension from the prostate and
seminal vesicles as is illustrated in our case.
Due to the inflammation of the scrotum and testes, it can be difficult to differentiate between
malignancy and inflammatory processes, such as a chronic infection. Physical exam may demonstrate
nodular beading of the vas deferens, which is a characteristic finding. Ultrasound of the scrotum can
help to differentiate an inflammatory process from malignancy or torsion.
The presence of scrotal pain, swelling, epididymal or prostate tenderness in the setting of TB should
prompt investigation of genital tract involvement. The positive AFB stain in our patient rapidly alerted us
to the presence of M. tuberculosis. Of note, acid fast microscopy can occasionally be positive due to
nonpathogenic, non-tuberculous mycobacterium. A culture of the biopsy or drainage is thus required for
the diagnosis. Culture has a sensitivity of 65% and a specificity of 100%.
[Date]
Testicular tuberculosis is a rare condition, but should be kept on the differential when evaluating scrotal
masses or infection. A thorough history, physical exam, and awareness of presentation can lead to the
accurate diagnosis.
108
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Nicole Barberis, MD
Fact or Factitious
First Author: Nicole Barberis, MD Second Author: Shagun Dhaliwal, MD Third Author: Tuan Tran, MS3
Necrotizing autoimmune myopathy (NAM) is a complex and rare disease under the umbrella of
idiopathic inflammatory myopathies (IIM), which includes the more common diagnoses polymyositis,
dermatomyositis, and inclusion body myositis. Patients typically present with sub-acute symmetrical
weakness of the limb girdle muscles, elevated serum creatine kinase (CK) levels, and absent
inflammatory cells on muscle biopsy. We present a patient with a persistent history of proximal muscle
weakness and dysphagia who’s muscle biopsy revealed acute necrotic myopathy.
A 57 year old female with a history of obesity, fibromyalgia and intermittent muscle weakness presented
with an acute worsening of her symptoms. Her first episode had been attributed to infectious myopathy
versus factitious or psychosomatic disorder. The workup included a CK 897, negative acetyl-choline
receptor antibodies, and a normal brain MRI. She had a sudden and complete recovery. Four months
later her proximal muscle weakness returned, with episodes where her legs “gave out” resulting in her
lying on her floor for two days. She was hospitalized and further evaluation revealed a CK of 218 but an
otherwise negative workup that included ANA, ferritin, Scr, TSH, cortisol, hepatitis panel, and CT head.
The consulting neurologist suggested she may have inclusion body myositis, but no biopsy was
performed. She was discharged to rehab where she resided for 3 months with some improvement
initially. However, she again had an acute worsening of her weakness and presented to our hospital with
a CK 1953, CRP 27, AST>ALT (318 and 164, respectively). Her muscle biopsy was consistent with
necrotizing myopathy.
For clinicoserologic classification, we sent anti-SRP and anti-HMGCR antibodies to evaluate necrotizing
autoimmune myopathy (NAM), in addition to an autoimmune myositis panel; all of which were negative.
She noted considerable improvement after treatment with prednisone 1mg/kg and a 5 day course of
400mg/kg IVIG. NAM is relatively rare and to date has only been described in few case reports since the
antibody discovery in the 1980’s. The etiology of NAM has yet to be fully delineated but has been
broadly divided into nonautoimmune (toxic, hypothyroidism, or heritable) and autoimmune myopathies
(anti-HMGCR, anti-SRP antibodies, antisynthetase, scleroderma as well as paraneoplastic antibodies).
[Date]
3-6% of patients with IIM have anti-SRP versus 16% in confirmed necrotizing myopathy while 6% have
anti-HMGCR. Statin-induced NAM is commonly associated with positive anti-HMGCR and although our
patient had a remote history of statin use, she was found to have neither anti-HMGCR or anti-SRP
antibodies. We believe the cause of our patient's myopathy was likely not toxin (statin, alcohol, etc..)
induced as it occurred while under clinical observation (rehab, hospitalization). It is likely that our
patient's symptoms were due to an as yet un-identified autoimmune process. It is important to note the
treatment of NAM is similar regardless of etiology, with recommendation to treat with at least
corticosteroids as well as IVIG or immunomodulator therapy in more severe cases.
109
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Cara E Crouch, MD
Acute hepatitis C infection transmitted by cadaveric bone graft transplantation
First Author: Cara E Crouch, MD Second Author: Miriam Freundt, MD
Introduction: Cadaveric bone graft transplants are commonly used in spinal surgery. Donors are
routinely screened for chronic hepatitis and other viral infections using antibody mediated laboratory
testing.
Case Description: A 51 year-old female school teacher presented to the hospital after a routine postoperative clinic visit revealed significantly elevated AST and ALT > 3000U/L. She had undergone bilateral
L4/L5 laminotomy with L4/5 diskectomy and interbody fusion with structural allograft and autograft 6
weeks prior. She admitted to worsening abdominal pain, nausea, vomiting and fatigue over the past
week. Her history was negative for sick contacts, recent travel, alcohol or drug use, sexual activity within
the last year, or previous blood transfusions. Physical exam was unremarkable. A RUQ ultrasound with
doppler revealed markedly thickened gallbladder walls with trace free fluid near the gallbladder without
evidence of stones, common bile duct dilation or abnormal liver flow. Extensive laboratory workup was
negative, including acetaminophen and salicylate levels, lipase, iron, TIBC, % iron saturation,
ceruloplasmin, anti-smooth muscle antibodies and ANA, as well as antibody testing for hepatitis A, B and
C (HAV IgM, HBV core IgM, HBV surface antigen, HCV antibody) as well as HSV I/II combined IgM, CMV
IgM, and EBV antibody panel. She was noted to have an elevated LDH and ferritin during workup. Given
the inconclusive nature of the results, HCV RNA PCR was checked and found to be positive, genotyping
revealed HCV genotype 2b. Her history was reviewed further to assess for any risk factors for HCV
infection, none were found except for previous cadaveric bone graft transplant. She was started on
sofosbuvir and ribavirin and on 2-month follow up HCV RNA levels were undetectable.
[Date]
Discussion: Acute HCV infection is an important cause of elevated liver function tests, and often
progresses to chronic infection with subsequent risk for cirrhosis and malignancy. Tissue donor
screening is currently mandated by the U.S. Food and Drug Administration to include testing for the
presence of HCV antibodies but not nucleic acid testing for HCV RNA and donors with acute HCV
infections may be missed. This case involves a patient without risk factors for HCV infection other than
her prior spine surgery and reinforces awareness for the risk of HCV transmission with tissue
transplantation. It is important to be aware that lack of RNA testing can result in transmission of HCV
and that this should be considered in post-operative patients with clinical and laboratory pictures that
resemble an acute HCV infection, as early treatment can lower rates of seroconversion.
110
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Miriam Freundt, MD
Invasive Rhizopus infection originating from the chest cavity post pneumonectomy
First Author: Miriam Freundt, MD Co-Authors: Assad Haneya, MD, PhD Stephan Hirt, MD, PhD Christof
Schmid, MD, PhD
Introduction: Rhizopus belongs to the family of Mucuraceae. As common saprobic fungus, it is found on
organic produce. Opportunistic zygomycosis occurs with diabetic ketoacidosis, haematological
malignancies, or severe immunosuppression.
Case Description: A 63 year-old male with diabetes mellitus (DM) and prostate cancer developed
squamous-cell carcinoma of the left (LUL) and right upper lobes (RUL). After 4 cycles of radiochemotherapy he underwent interval VATS for atypical RUL wedge-resection and LUL cuff resection. On
post-operative day (POD) 2 acute respiratory failure due to total occlusion of the left pulmonary artery
prompted left pneumonectomy. Due to diffuse oozing the chest was packed with 11 laparotomy
sponges. Worsening septic shock required maximal vasopressor support. On POD 5 the chest was depacked, irrigated with povidon-iodine and closed. Cultures from pericardium, chest and sputum
remained sterile. Blood cultures grew Staph. epidermidis and antibiotics were broadened. A chest tube
drained black fluid positive for 2 different Rhizopus species (R. microsporus and azygosporus). IV
posaconazole and liposomal amphotericin B were initiated. The chest was frequently rinsed with saline.
On POD 8 necrosis of the incision was noted. Within days the necrosis expanded to a palm sized area.
Samples revealed generalized invasive zygomycosis. Extensive debridement of pericardium, pleura and
chest wall with resection of 4 rips was performed. Invasion of the aorta, heart and bronchus stump
could not be excised. Following the family opted for comfort-care and the patient expired.
[Date]
Discussion: This case represents the fatal outcome of Rhizopus infection originating and hiding in the
chest after pneumonectomy. Our patient expressed no typical risk factors. Immunocompromise due to
repeat surgery, bacteremia and radio-chemotherapy might have been present but DM was controlled.
The source of infection remains unclear. The chest cavity offered ideal environment for this aggressive
opportunistic mold and invasion was only noted when outgrowing from surgical incision. Hallmark of
zygomycosis is vascular invasion and tissue necrosis, which occurred rapidly despite IV combination
antimycotic therapy. At surgical intervention, the large vessels and heart had already been invaded. We
reinforce the need for early removal of chest packing, awareness of invasive zygomycosis, timely
diagnostic tap with fungal stains and recommend local irrigation with amphotericin B after early radical
surgical debridement.
111
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Miriam IE Freundt, MD
Amiodarone Desensitization by a Novel Protocol in a Patient with Advanced
Biventricular Heart Failure and Uncontrolled Ventricular Tachycardia
First Author: Miriam IE Freundt, Second Author: Francis C. Ngo, MD
Introduction: Patients with advanced cardiomyopathy are prone to ventricular tachycardia (VT).
Amiodarone is first choice treatment and therapy-limiting allergic reactions are extremely rare.
However, we present a case of refractory polymorphic VT with amiodarone as last resort but
generalized amiodarone-induced dermatitis, which was successfully desensitized by our novel protocol.
Case Description: A 66 year-old male with idiopathic cardiomyopathy (left ventricular ejection fraction
15%), left bundle branch block, remote cardiac arrest due to VT, biventricular AICD and lymphoma
experienced recurrent symptomatic polymorphic VT requiring shocks ultimately climaxing in electrical
storm. Historically he had been unable to tolerate amiodarone due to a generalized rash supportive of a
delayed non-IgE mediated dermatitis, which had resolved after discontinuation. Allergies included rash
to triamterene, triamcinolone and losartan but no anaphylaxis. Dofetilide, mexiletine and metoprolol
were at maximal doses, AICD settings optimized, and other available antiarrhythmic medications had
failed. Amiodarone desensitization was pursued in the intensive care unit. Dofetilide had been
discontinued and metoprolol held for 18 hrs. The following protocol was instituted: Pretreatment with
125 mg methylprednisolone and 20 mg famotidine once 4 hours before the first amiodarone dose. A
cumulative dose of 150mg of amiodarone was infused at potentiating dosage each in 50 ml dextrose 5%
over 15 mins, and then waited for 15 mins before the next dose. Starting dose was 0.008 mg, followed
by 0.02 mg, 0.04 mg, 0.08 mg, 0.2 mg, 0.4 mg, 0.8 mg, 1.6 mg, 4 mg, 8 mg, 16 mg, and 120 mg. No
adverse reactions occurred. 400 mg amiodarone daily were started and he was discharged home in
stable condition. Unfortunately he was readmitted two days later for recurrent VTs, again requiring
multiple AICD shocks. VT could be stabilized with amiodarone infusion and three boluses of 150mg. He
eventually received a left ventricular assist device for destination therapy and was continued on
amiodarone.
[Date]
Discussion: In this case break through VT and impending hemodynamic instability on exhausted medical
therapy required intervention. Ablation had been discussed at that point but seemed too dangerous
without hemodynamic LVAD support. Due to the patient’s history of severe generalized rash, concern
for anaphylaxis to amiodarone prompted the need for desensitization. To our knowledge no such
protocol has previously been described. Successful amiodarone desensitization using our novel protocol
is encouraging for similar cases, where amiodarone remains the only antiarrhythmic option despite
previous allergic reactions.
112
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Kelsi Lacock, MD
Pulmonary mucormycosis in a diabetic patient: an unusual presentation.
First Author: Kelsi Lacock, MD Second Author: Cara Crouch, MD – Saint Joseph Hospital, Denver, CO
Introduction: Mucormycosis is an opportunistic fungal infection that typically presents as rhino-cerebral
disease in diabetic patients. We present a case of this rare infection diagnosed in a patient with poorly
controlled diabetes mellitus (DM) who developed primary pulmonary disease and challenging adverse
effects from the currently available treatment options.
Case Description: A 57 year-old male with past medical history of poorly controlled DM initially
presented to his outpatient physician for chronic productive cough, was found to have a cavitary lesion
within the right lower lobe (RLL) and was prescribed two months of amoxicillin/clavulanate. Follow-up
imaging demonstrated improvement in the RLL abscess but identified a new abscess in the right middle
lobe (RML) prompting his admission to the hospital. His history also included night sweats and an
unintentional 80lb weight loss over the previous 6 months. Physical exam was only significant for
decreased breath sounds at the right lung base. Labs included blood glucose >400 without acidosis and
hemoglobin A1C of 13.1; the remainder of his laboratory workup was negative. A thoracic CT revealed
two abscesses within the RML, 5cm and 1.5cm in diameter, as well as a thick walled right-sided pleural
effusion. He underwent bronchoscopy with brushings and cultures consistent with mucormycosis. He
was treated with amphotericin B lipid complex and underwent surgical resection of the RML. Pathology
confirmed mucormycosis without evidence of vascular invasion. Treatment was complicated by the
development of rigors during amphotericin infusion as well as acute kidney injury. He was maintained
on amphotericin B for 3 weeks post-operatively and then transitioned to posaconazole for 3 months at
discharge. He subsequently developed anasarca thought secondary to posaconazole that required readmission and resolved with diuretic therapy.
[Date]
Discussion: Mucormycosis is an extremely aggressive angioinvasive fungal infection. Incidence of
reported cases has been decreasing in diabetic patients, and these patients most often develop rhinocerebral disease and are typically found to have concomitant diabetic ketoacidosis at
presentation. Primary pulmonary mucormycosis is more commonly seen in patients with hematologic
malignancies and neutropenia. This case involves a patient with poorly controlled diabetes who
developed a primary pulmonary infection, demonstrating the need to keep this diagnosis within the
differential of a patient with persistent respiratory complaints. This case also highlights the complicated
nature of the treatment regimen, which is often plagued by medication side effects occasionally
requiring hospital readmission. Early recognition and treatment with combined IV antifungal agents and
surgical resection is imperative for achieving improved outcomes in this rare, and often fatal, infection.
113
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Michael Lam, MD
Recurrent stroke-like symptoms in a patient with recent trigeminal zoster
First Author: Michael D. Lam, MD Second Author: Michael T. Morton, MD, FACP
Introduction: Varicella zoster virus (VZV) is a well-known cause of primary chicken pox, or reactivation
zoster. However, it may present atypically as well. We present a case of recurrent ischemic strokes for
which the etiology was VZV infection.
Case Presentation: A 58 year old woman with past history of bipolar disorder, chronic kidney disease,
stage III, and diabetes mellitus, presented to the hospital with 3 weeks of intermittent confusion and
apraxia. Seven weeks prior to admission, she was diagnosed and treated for left-sided trigeminal zoster
and zoster opthalmicus, with her current symptoms developing at the completion of her antiviral
therapy. Physical exam on arrival was significant for word finding difficulty, disorientation, apraxia and
agnosia. The remainder of her exam was normal. Initial studies, including CT of the head, lumbar
puncture, and echocardiography, were unremarkable. MRI of the brain showed abnormal signal
diffusion in the left deep grey nuclei and left basal ganglia (ipsilateral to her recent zoster). A CT
angiogram was performed which showed vascular narrowing at proximal left A1 and M1 segments of
the cerebral arteries that may be seen from vasculopathy or an embolic event. Given her recent VZV
infection and the temporal relation of the patient’s symptoms, VZV vasculopathy was
investigated. Subsequent testing of the patient’s CSF was positive for VZV IgM and IgG, although
negative for VZV-PCR. Treatment for VZV vasculopathy was initiated with high dose steroids and a 2
week course of intravenous acyclovir. She showed dramatic neurologic improvement and was
discharged.
Subsequently, the patient had two more presentations to the ED with similar cognitive complaints, as
well as new right-sided motor weakness. Repeat workup ruled out infectious, epileptic, cardiac,
embolic, metabolic or toxic causes of her recurrent symptoms. Repeat MRI showed numerous small
acute on chronic ischemic strokes in the distribution of the left middle cerebral artery, thought to be
due to persistent VZV vasculopathy and associated vasospasm. She was prescribed a two-month course
of antiviral therapy as well as nimodipine for treatment of vasospasm. Her symptoms improved prior to
discharge, but unfortunately, she was then lost to follow-up.
[Date]
Discussion: VZV vasculitis is a rare entity seen either in primary VZV infection (typically children) or in
reactivation of latent infection (adults or immunosuppressed patients). Case reports have shown that
VZV affects both small and large vessels thus providing a broad spectrum of clinical presentations
ranging from broad hemiplegia, to subtle, transient manifestations. VZV vasculitis should be considered
as a potential etiology in ischemic stroke when more common causes are absent. Diagnosis is critical to
allow quick initiation of treatment to prevent further morbidity and mortality.
114
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Lauren B Miller, MD
The Metamorphosis: One Tumor’s Tale of Transformation
First Author: Lauren B Miller, MD Second Author: Brittany R Folks, MD
Introduction: Patients with MEN1 syndromes have occasionally been found to have neuroendocrine
tumors that simultaneously or sequentially secrete different hormones, however each hormone is
typically produced by a separate and pathologically distinct tumor. Multiple hormones co-secreted by a
single neuroendocrine tumor are exceedingly rare.
Case: A 54 year old woman with a 3 year history of a gastrin-secreting neuroendocrine tumor
(gastrinoma) with metastases to the liver, bone, and adrenal glands presented to the Emergency
Department with several weeks of intermittent altered mental status associated with dizziness and
nausea. On the morning of presentation, she had an episode of seizure-like activity and was found to
have a blood glucose level of 20mg/dL during EMS transport. Upon arrival to the hospital, her blood
glucose level had risen to 50mg/dL following dextrose administration. Several additional doses of
dextrose and a dextrose drip were required to maintain her blood glucose levels above 100mg/dL. She
became asymptomatic once normoglycemia was achieved. A pro-insulin level of 99pmol/L, insulin level
of 30uIU/mL, and C-peptide level of 3.9ng/mL with a negative sulfonylurea screen and a corresponding
glucose of 54mg/dL was consistent with insulinoma. CT imaging of her abdomen and pelvis did not
demonstrate the presence of new tumor burden. She was initially treated with prednisone followed by
octreotide. She maintained her glucose above 70mg/dL for 48 hours, and both therapies were continued
for ongoing treatment at the time of discharge.
[Date]
Discussion: Insulinomas are thought to arise from the ductal/acinar system of the pancreas. The
majority of tumors are benign, but some have malignant potential. The diagnosis of an insulinoma is
made when inappropriately elevated insulin levels are found in the presence of symptomatic
hypoglycemia. Serum insulin greater than 5uIU/mL, C-peptide level greater than 0.2ng/mL, pro-insulin
levels greater than 5pmol/L, and a corresponding glucose less than 55mg/dL are suggestive of the
diagnosis. Although the most definitive treatment is tumor resection, diazoxide and somatostatin
analogs are reasonable choices in those unable to undergo surgery. The presence of discrete
neuroendocrine tumors that secrete different hormones in the same patient are very unusual,
particularly in the absence of MEN1. It is exceptionally uncommon for dual-secretion to occur from the
same tumor. Our patient had never undergone testing for MEN1 gene mutations, however, she had no
significant family history and no evidence of additional malignancies. Imaging during this admission was
not significantly changed from previous, and it was the consensus of oncology and endocrinology that
her overall clinical picture was most suggestive of a transformation of her gastrinoma into a co-secreting
insulinoma.
115
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Tyler Miller, MD
Systemic Amyloidosis Presenting as Acalculous Cholecystitis
First Author: Santiago Rodriguez, Tyler Miller, Rachel Groff
Case: A 77 year-old male with a history of coronary artery disease, heart failure, and chronic kidney
disease was transferred to our hospital with several weeks of generalized weakness and abdominal pain
without fever, jaundice, or weight loss. Initial examination was notable for normal vital signs, normal
heart and lung sounds, and prominent right-upper quadrant tenderness. CT of the abdomen revealed a
hydropic gallbladder without gallstones. He was referred for cholecystectomy; however pre-operative
laboratory testing revealed a creatinine of 6.5 (baseline 2.1), a troponin of 8.2, and a BNP of 2538. He
was admitted for acute kidney injury and non-ST elevation MI. He was treated for these conditions, and
was able to proceed to cholecystectomy several weeks later. The patient’s creatinine improved to 4.3
but never returned to his prior baseline. This prompted further workup including serum light chains
which demonstrated a markedly abnormal kappa-to-lambda ratio of 4.8. Histopathological examination
of the patient’s gallbladder revealed diffuse apple-green bifringence using Congo red staining. A
diagnosis of systemic amyloidosis was made. Unfortunately, the patient went on to develop recurrent
heart failure symptoms several months later suspicious for cardiac amyloidosis. Echocardiography at this
time demonstrated global hypokinesis, left ventricular hypertrophy, and echotexture consistent with
amyloid cardiomyopathy. He was able to continue chemotherapy and return home; however, his overall
prognosis remains poor.
Discussion: Amyloidosis refers to the extracellular deposition of abnormal insoluble protein fibrils,
leading to disruption of normal tissue and eventually organ dysfunction. Infiltration of the heart, kidney,
and liver are the common clinically evident manifestations of the disease. Clinically significant
involvement of the gallbladder is extremely unusual. There are only four prior reported cases of
amyloidosis presenting as acalculous cholecystitis. Other reported variants include patients with
nonspecific gastrointestinal symptoms, hemorrhage, and an asymptomatic patient in whom gallbladder
cancer was suspected. Tissue biopsy is the only way to confirm amyloidosis, but several other clinical
manifestations may raise suspicion for the diagnosis. These most commonly include unexplained
progressive heart failure, nephrotic syndrome, and macroglossia. In retrospect, our patient had kidney
and heart involvement at the time of his initial presentation. However, the diagnosis was not suspected
until he developed worsening organ failure. Treatment depends on the type of amyloidosis, but long
term prognosis is poor for most cases.
[Date]
Conclusion: We report a case of systemic amyloidosis presenting as acute cholecystitis. This is a highly
unusual presentation with only four prior documented cases. The clinical presentation of amyloidosis is
variable, but may be considered particularly in cases of unexplained concurrent heart or kidney failure.
116
COLORADO POSTER FINALIST - CLINICAL VIGNETTE Muthulakshmi Yegappan, MD
TACEred Into Paralysis
1st author: Muthulakshmi Yegappan, 2nd author: Thomas Seibert, 3rd author: Aaron Calderon
Introduction: Hepatocellular carcinoma (HCC) is the fifth most common solid organ malignancy. It is
often found in advanced stages requiring palliative rather than curative therapy. Trans-catheter arterial
chemoembolization (TACE) is commonly offered as a treatment option to non-operative patients. We
describe a rare case of cerebral embolization following TACE.
Case: A 69 year old male with history of hepatitis C and hepatocellular carcinoma was admitted for
planned palliative TACE. The procedure was uneventful: right hepatic arteries were accessed via right
common femoral artery and Adriamycin impregnated LC beads mixed with ethiodol followed by one vial
of 100-300 micron embospheres, were introduced with successful interruption of blood flow to the
tumor. Later that evening the patient became acutely confused and had difficulty moving his left arm
while progressively becoming more somnolent. CT head revealed multiple areas of ischemic changes in
the subcortical white matter and cerebellum, and MRI confirmed too numerous to count acute embolic
infarcts. Once his mental status improved, a dense left hemi-paresis was uncovered and an
echocardiogram revealed the presence of a patent foramen ovale (PFO). It was hypothesized that the
chemoembospheres travelled through an intra-tumor arteriovenous malformation, although one was
not visualized on arteriogram during the procedure. The embospheres then entered the venous
circulation and passed to left heart circulation via a PFO and/or aberrant pulmonary arterial-venous
shunts resulting in embolic cerebral infarcts. During his hospital course he also developed respiratory
distress with multifocal opacities on chest radiograph. This was thought to be from chemoembolization
to the lungs and aspiration pneumonia. He slowly improved and was discharged to a rehabilitation
facility with almost normal mental status, left upper extremity hemiparesis, and left lower extremity
hemiplegia.
[Date]
Discussion: Cerebral embolization after TACE is a rare disorder that clinicians should become familiar
with. An extensive literature review revealed only 15 cases, however, as the procedure becomes more
common, increased events can be expected. Patients typically develop neurologic symptoms during the
procedure or soon after. While most patients can anticipate a full recovery, the condition can be
fatal. Known risk factors for cerebral embolization after TACE include pulmonary AVMs, repeat
embolization, and tumor AV shunt. We suggest that patients with a PFO are at very high risk for cerebral
embolism after TACE and that routine screening be considered given that the prevalence of a PFO
approaches 25% in the adult population. At the very least, in patients with advanced tumors and
significant risk factors for cerebral embolization, alternative treatment strategies should be considered.
117
CONNECTICUT POSTER FINALIST - CLINICAL VIGNETTE Bhavtosh Dedania, MD
Ulcerating Skin Lesions, Cocaine and Levamisole
First Author:Dipen Khanapara, MD Second Author:Amruta Panwala, MBBS Third Author: Bhavtosh
Dedania, MD Fourth Author: Edgar Naut R, MD.
Learning Objective: Recognize levimasole as a common etiology of vasculitis in cocaine abusers.
Understand the appropriate work up for levimasole induced vasculitis
Introduction: An estimated more than two thirds of the cocaine used in the United States is
contaminated with levamisole. Due to its immunomodulatory action, levamisole has been used in the
past for rheumatoid arthritis, colon cancer, and pediatric nephrotic syndrome. It is currently used for
the treatment of nematode infections in animals. We report a case of skin lesions induced by levamisole
contamination of cocaine.
Case: A 28 year old female with active IV drug use presented multiple times to the hospital with painful
ulcerating lesions on her nose, right breast, hands, legs, and undersurface of the tongue. She had a long
standing history of cocaine abuse, having tested positive for cocaine on toxicology screens multiple
times in the past five years. Her WBC counts ranged from 4.7 to 7.4 x 109/L while the rest of her
bloodwork was normal with negative blood cultures. Skin lesions biopsies showed skin, subcutaneous,
and connective tissue necrosis. Skin and subcutaneous tissue showed organizing thrombosis, ulceration
and reactive epidermal changes. Immunofluorescent studies of the tissue were negative for IgG, IgM,
IgA, C3 and fibrinogen. She was eventually tested for levamisole using chromatography tandem mass
spectrometry. These results showed a positive levamisole level of 0.39 mcg/ml. She was discharged after
counseling on strict cocaine abstinence. Between her multiple admissions, resolution of these lesions
were noted with cocaine abstinence
Discussion: Levamisole is currently used as a “cutting” or debulking agent to increase the total weight of
street cocaine. It modulates the immune response by triggering macrophage chemotaxis and increasing
T-cell lymphocyte function. Patients with levamisole-induced toxicity usually present with skin
manifestations or joint pain. The exact pathology is unclear as patients may present with true vasculitis
or pseudovasculitis. Leukopenia, neutropenia, and agranulocytosis are very common lab abnormalities
seen in such patients. . Urine toxin screen typically is positive for cocaine for approximately 72 hours
after last use. Levamisole needs specialized testing and it is positive for less than 48 hours after last use.
Antihuman elastase antibody level is a sensitive and specific test for levamisole-induced vasculitis. The
natural progression of this condition is generally benign, complete clinical resolution of skin lesion
occurs 1 to 3 weeks after stopping levamisole exposure.
[Date]
Conclusion: Increased physician vigilance is essential to suspect exposure to levamisole-contaminated
cocaine. Any known IV drug using patients, when presenting with an unexplained rash, neutropenia, and
multiple immunological abnormalities should be tested for cocaine and levamisole.
118
CONNECTICUT POSTER FINALIST - CLINICAL VIGNETTE Birinder S Singh, MD
Anti-NMDA receptor encephalitis: A Potentially Fatal Autoimmune Encephalitis
Birinder S Singh, MD, Sartaj S. Sandhu, John G. Stratidis, John J. Chronakos, Behzad H. Khameneh
Introduction: Anti-NMDA (N-Methyl D-aspartate) receptor encephalitis is a rare form of an acute
autoimmune process that is more prevalent in young females with a possible association with ovarian
teratomas. This condition may initially present as a prodromal viral-like illness with multi-stage
progression of symptoms. The presentation usually includes prominent psychiatric manifestations such
as agitation, bizarre behavior, hallucinations amongst other symptoms like autonomic instability,
insomnia, and memory impairment. This is followed by decreased level of consciousness that is often
fatal without timely intervention.
Patient Description: Our case is of a 30 year old female, with no significant past medical history, who
presented with a few days of confusion, agitation, bizarre behavior and hallucinations. Lumbar puncture
showed mild lymphocytic pleocytosis. MRI of the head showed nonspecific sulcal flair signal
hyperintensity. She was started on acyclovir for possible viral meningoencephalitis. In the next few
days, her mental status deteriorated and she had become minimally responsive. Her oxygen saturations
dropped and an ABG revealed hyper-capnic respiratory failure requiring an emergent intubation and an
ICU transfer. In the ICU, the patient was worked up for autoimmune and infectious causes for this
possible encephalitis. The patient was also found to have episodes of choroathetoid movements of her
upper and lower extremities on the left side, oro-facial dyskinesias, rigidity and opisthotonic posture. A
repeat brain MRI showed resolution of the previously seen hyperintensity. At this point, she was
presumed to have anti-NMDA receptor encephalitis based on the clinical presentation and the multistage evolvement of symptoms. She was started on high dose of methylprednisolone and intravenous
immunoglobulin (IVIG). Cell binding assay for NMDA receptor antibody was reported positive. We
followed the treatment protocol developed by Dalmau et al. The patient’s tumor (ovarian teratoma)
was removed and she received a five-day course of methylprednisolone and IVIG. She continued to
experience episodes of extreme agitation and seizures. Her symptoms began to improve after three
doses of rituximab. She continued to show slow recovery on immunosuppressive therapy.
[Date]
Conclusion: Anti NMDA receptor encephalitis is an autoimmune condition with limited understanding
of the underlying pathology. Various theories hypothesize that antibodies directed against synaptic
proteins are the likely offenders. As we become more familiar with this condition, timely recognition
and appropriate intervention is of paramount importance. A high index of suspicion is warranted in
young healthy patients presenting with encephalitis associated with psychotic features and
dyskinesias. Our case highlights the limited literature available on anti NMDA receptor encephalitis
recognition and treatment. It is therefore prudent to become familiar with the symptomology to offer
timely intervention.
119
CONNECTICUT POSTER FINALIST - CLINICAL VIGNETTE Jin Xu, MD
Allopurinol-induced Giant Cell Hepatitis
First Author: Jin Xu Second Author: Stephen Harden Third Author: Albert Do Fourth Author: Lisa Puglisi
A 66-year-old woman with a history of RAI Stage 1 chronic lymphocytic leukemia (CLL), on active
observation, presented to her outpatient physician with abdominal discomfort and mild
transaminasemia ten days after initiating allopurinol for hyperuricemia. Allopurinol was discontinued
and she was hospitalized one week later when laboratory testing revealed markedly worsening liver
chemistries. She was discharged after 3 days when serial laboratory testing showed a stable downtrend
in liver chemistries, however was readmitted 6 days later with dramatic re-uptrend in liver chemistries.
Her physical examination was notable for jaundice, splenomegaly and hepatomegaly without skin rash
or mental status changes. Laboratory testing revealed a white blood cell count 238,000 cells/uL with
85% lymphocytes (baseline 65,000 cells/uL with 70-80% lymphocytes) but no eosinophilia and normal
basic chemistries. Liver chemistries were significant for alanine aminotransferase (ALT) 4,310 U/L,
increased from 1,950 U/L one week prior, 237 on initial presentation and normal at baseline. Total
bilirubin peaked at 18.2 mg/dL, with international normalized ratio (INR) 1.2 and normal albumin and
platelets. Further testing for viral hepatitis, autoimmune hepatitis, cytomegalovirus (CMV), Epstein-Barr
virus (EBV), Human herpesvirus-6 (HHV-6), and acetaminophen toxicity was unrevealing. There was no
evidence of biliary or vascular obstruction on abdominal ultrasound with Doppler and magnetic
resonance cholangiography. Liver biopsy ultimately revealed giant cell transformation of hepatocytes.
There was no evidence of steatosis, siderosis, cholestasis, or granulomas. There were portal lymphoid
infiltrates consistent with known CLL.
Due to concern for rapidly progressive liver injury, she received five days of oral N-acetylcystine (NAC).
When bilirubin continued to uptrend, oral prednisone 60 mg per day was initiated with gradual
improvement. Prednisone was subsequently tapered, and on follow up 2 months later the patient was
asymptomatic with normalized liver chemistries and WBC was at her baseline.
[Date]
We describe a patient with acute liver injury after allopurinol initiation, manifesting as giant cell
hepatitis rather than the typical presentation of allopurinol-induced liver toxicity. Most cases of
allopurinol-induced liver injury are thought to be due to a hypersensitivity reaction, manifesting with
rash, eosinophilia, and systemic symptoms (DRESS syndrome). Clinical manifestation can range from
isolated laboratory abnormalities to fulminant liver failure and death. Similarly, the clinical course of
giant cell hepatitis, a histopathological entity not previously described with allopurinol-induced liver
toxicity, is often fatal or of transplant-dependent severity. Early suspicion/recognition and prompt
discontinuation of allopurinol, as well as expedient initiation of NAC and steroids, may affect the clinical
course favorably.
120
DELAWARE POSTER FINALIST - CLINICAL VIGNETTE Akash N Sethi, DO
It Will Take Your Breath Away - A Case Of Rapidly Progressing Pulmonary Tumor
Thrombotic MIcroangiopathy
Akash Sethi DO, Badrish Patel MD
INTRODUCTION: Pulmonary tumor thrombotic microangiopathy (PTTM) is a rare but lethal diagnosis. It
is a rapidly progressing disease associated with metastasizing tumor cells that cause sudden dyspnea,
severe right sided heart failure and ultimately hemodynamic collapse.
CASE PRESENTATION: A 40 year old female patient with no medical history presented after a brief
syncopal episode that was preceded by chest pain and dyspnea. Initial evaluation revealed a modestly
elevated troponin with right axis deviation on EKG that prompted a workup to rule out acute coronary
syndrome and pulmonary embolism. Cardiac catheterization revealed clinically insignificant myocardial
bridging while 2D echocardiogram was essentially normal. Chest CT angiography with good contrast
bolus showed no pulmonary embolus, but did show concerning axillary lymph nodes, which were
confirmed by needle biopsy to be metastatic breast cancer. The patient was stable and awaiting chemoport placement when she had sudden hemodynamic collapse requiring intubation and multiple
vasopressors. Bedside echo showed dilated right ventricle with severe pulmonary hypertension. Repeat
CTA again showed no PE so presumptive diagnosis of PTTM in light of confirmed malignancy was
made. A ventillation-perfusion scan showed extensive bilateral peripheral mismatched areas consistent
with PTTM. A pulmonary artery catheter was placed for hemodynamic monitoring in addition to starting
nitric oxide to offload the right ventricle. Unfortunately, despite best efforts, our patient had progressive
right heart failure and passed after prolonged PEA arrest. Post mortem autopsy confirmed the diagnosis
of PTTM in the setting of metastatic breast cancer along with malignant cells cultured from the tip of
the PA catheter.
[Date]
DISCUSSION: PTTM is a devastating disease in which tumor cells invade the pulmonary vasculature and
trigger the coagulation and inflammatory cascades. The pathophysiology, however, is not clearly
understood. The clinical scenario is rapidly progressing dyspnea and chest pain that can progress to
hemodynamic compromise and ultimately death. Diagnosis is usually clinical, but VQ scans may show a
peripheral mismatch not demonstrated by CTA as the affected vessels are generally the fourth and fifth
generation. Echocardiogram will typically show right heart strain and signs of pulmonary hypertension.
Depending on progression of symptoms, PET scanning or transbronchial biopsy may also help with
diagnosis. Anticoagulation and pulmonary vasodilators are of uncertain benefit at this time. The
malignancies that have the highest potential of PTTM are breast cancer, gastric adenocarcinoma and
lymphangiosis carcinamotosa. Several case reports have reported more indolent progression than with
our patient, but the overall mortality still remains high. The average life expectancy after diagnosis is a
mere 16.2 days. By increasing awareness of PTTM, more cases will be recognized and more antemortem
diagnoses will be made which is the first step toward fully understanding this deadly disease.
121
DELAWARE POSTER FINALIST - CLINICAL VIGNETTE Giovanna L Uzelac, MD
A Case of Ehrlichiosis: Going on A History and a Hunch
First Author: Giovanna L Uzelac, MD Second Author: John Piper, MD
Over the last 30 years, the incidence of tick borne illnesses has steadily increased. Significant morbidity
and mortality due to human monocytic ehrlichiosis (HME) has been documented. Oftentimes, clinicians
can only rely on their history, as tests for ehrlichiosis can take days to weeks to identify the causative
organism. Increased awareness of tick borne illnesses, especially in endemic areas, will lead to earlier
suspicion, diagnosis, and thus earlier initiation of appropriate therapy which can potentially decrease
the morbidity and mortality caused by tickborne diseases.
A 71-year old woman presented with 3-4 days of fever, weakness, and confusion after returning from a
trip to Chicago. She initially presented to her primary doctor who recommended supportive care for a
suspected viral syndrome. She continued to decline and presented to the emergency department, was
admitted, and treated for a suspected urinary tract infection. Laboratory studies also revealed a
leukopenia (white blood cell count 2.4k/uL), thrombocytopenia (platelet count 60,000) and mildly
elevated transaminases. Two days into her admission she was transferred to the ICU for respiratory
distress and concern for impending respiratory failure. Echocardiogram and VQ scan did not identify a
cause for her respiratory distress, and as her neurologic status also declined, there was a suspicion for a
meningoencephalitis. Cerebrospinal fluid demonstrated elevated protein and white blood cells, but also
many red blood cells. A more detailed history was obtained that included a possible tick bite several
weeks prior. She was empirically started on doxycycline. During the first 24-48 hours she worsened,
developing seizures that required transfer to the neurologic ICU. Rocky Mountain Spotted Fever IgG titer
was 1:512 on day 4 of doxycycline therapy. Despite negative IgM antibodies this was the leading
diagnosis until day 10 when Ehrlichia chaffeensis PCR returned positive. She continued to require ICU
level of care for multi-organ failure. She continued to require ventilator support until day 14 of
antibiotics and seizures were eventually controlled on antiepileptics. Most other lab studies returned to
normal except for her renal function, and she was discharged on dialysis.
[Date]
The onset of HME can be insidious or it can be fast, potentially fatal. Many times, early clinical signs are
nonspecific, resembling countless other diseases. Leukopenia, thrombocytopenia, and mild elevation in
transaminases can be helpful in making a presumptive diagnosis of ehrlichiosis. However, the most
important clues are in the patient history, which may provide the only clue to the diagnosis, although
many times a tick bite remains unnoticed. It is imperative for clinicians to recognize the possibility of
ehrlichiosis, to obtain appropriate diagnostic tests, and to initiate treatment with doxycycline promptly.
122
DISTRICT OF COLUMBIA POSTER FINALIST - CLINICAL VIGNETTE Munaza M Akunjee, MD
Barking Up The Wrong Tree: Recurrent Syncopal Episodes as The Presentation of
Coronary Vasospasm
First Author: Munaza Akunjee, MD Second Authors: Antonio Corona, MD and Kimia Ghaznavi, MD
Coronary artery vasospasm, associated with variant angina, is a well-documented disorder with
established methods of diagnosis and treatment. Clinical suspicion for this condition, however, remains
indefinite. While its presentation is similar to that of typical angina, there have been rare instances that
coronary vasospasm has presented with syncope. Here, we present a case of three-vessel coronary
vasospasm presenting as recurrent, syncopal episodes. This raises the question whether the term,
“variant angina”, remains appropriate as the designation of this condition.
Our patient is a 64 year old male who was brought to our institution by his sister for a witnessed episode
of syncope. He had an extensive medical history which includes hypertension, COPD, renal cell
carcinoma, colon cancer, as well as well-controlled generalized tonic-clonic seizures due to a traumatic
brain injury sustained 20 years earlier. The patient described preceding symptoms of flushing and
dizziness. No reports of chest pain, shortness of breath, palpitations, or seizure-like activity were made.
The patient claims that he had two similar incidents one month prior to his presentation. Physical
examination findings were unremarkable. A neurologic cause of his symptoms was investigated. A CT
scan of the head was done in the emergency department showing no acute findings. Laboratory studies
showed a complete blood count and comprehensive metabolic panel that were within normal limits. A
12-lead EKG showed no ischemic changes and no abnormal rhythms. Troponin-I levels were slightly
elevated at 0.054 ng/ml, however. Cardiac enzyme measurements were repeated, and Troponin levels
were discovered to be trending upwards to as high as 13.7 ng/ml. A series of 12-lead EKG’s were also
obtained showing 3mm ST segment elevations in the inferior leads lasting for 6 minutes before
returning to baseline. The patient remained asymptomatic during this time. The patient underwent
cardiac catheterization, which revealed severe coronary artery spasm of the left anterior descending,
left circumflex, and right coronary arteries. No angiographic evidence of epicardial coronary artery
disease was found. Intracoronary nitroglycerin was infused, relieving the vasospasm. Isosorbide
mononitrate and amlodipine were initiated and the patient remained symptom-free and stable. He was
discharged in stable clinical condition. He has since followed up one month after his admission with no
recurrence of syncope.
[Date]
Our case illustrates how variant angina can be an inaccurate representation of coronary vasospasm.
Reports of syncopal episodes, with the underlying mechanism hypothesized to be ventricular
arrhythmias, have been made. This case seeks to shed light on the different symptoms coronary
vasospasm can present with, which are not limited to angina, and the need to recognize them.
123
DISTRICT OF COLUMBIA POSTER FINALIST - CLINICAL VIGNETTE Ahmed Babiker, MBBS
Redefining Tropical Pyomyositis: A Case of Pyomyositis of the Pectoralis Major in
an Immunocompetent Adult
First Author: Ahmed Babiker, MBBS Co- Author: Antonio Corona, MD
Pyomyositis has historically been associated with pyogenic infections of the skeletal muscles of the
lower extremities, immune deficient states, and being endemic to tropical countries. Documented case
reports from this past decade, however, are changing how this infection is viewed. Our case illustrates
how our classic definition of pyomyositis needs to evolve, and be considered in the differential
diagnosis of patients presenting with fever and muscle pain.
A 25 year-old previously healthy male was seen at our urgent care department for complaints of left
chest wall muscular pain he had been experiencing for about a week. At that time, the patient related
the symptoms to his work as a porter at a local grocery. The patient had no history of HIV or
immunosuppression, no IV drug abuse, no recent travel and no previous hospitalizations. He had no
visible skin breaks on examination. He was given ibuprofen for pain relief and was discharged home. The
patient returned to our institution 11 days later, complaining of worsening pain and swelling of his left
chest wall, now associated with fevers and chills. A CT scan with IV contrast of the area revealed a
diffusely enlarged pectoralis major muscle with inflammatory stranding, but with no evidence of abscess
formation. Treatment with intravenous cefazolin was initiated, however, the patient’s condition
worsened during the succeeding hospital days. As a result, an MRI of his chest was done which revealed
a complex, multiseptated collection in the lateral inferior aspect of the left pectoralis major muscle. A
left chest wall incision and drainage was then performed yielding purulent material as well as several
blood clots. The blood clots were suspicious for underlying trauma the patient had sustained related to
his work. Culture reports from the drainage were found to grow MRSA. Blood cultures and nasal swabs
obtained from admission were found to be growing MRSA, as well. His antibiotic was then changed to
vancomycin. Thereafter, the patient had marked improvement clinically. He was discharged home
improved and stable, with IV antibiotics to complete 14 days. He has since followed up at our outpatient
services with complete resolution of symptoms.
[Date]
The above case demonstrates a case of pyomyositis occurring in the pectoralis major in the absence of
immunosuppression. Although preceding trauma and community acquired MRSA colonization are two
well-documented risk factors for this disease, the pathophysiology behind this purulent infection is not
fully understood. As pyomyositis continues to be increasingly recognized in temperate climates,
physicians should be more vigilant to this disease entity as early recognition and institution of
appropriate management are crucial to avoid severe complications.
124
DISTRICT OF COLUMBIA POSTER FINALIST - CLINICAL VIGNETTE Joseph J Jennings, MD
Help! My ACLS Algorithm Isn’t Working!
Joseph Jennings, MD
CASE PRESENTATION: A 52 y/o male with documented severe CAD s/p multiple percutaneous coronary
interventions (PCIs) presents with a 3-day history of chest pain that has acutely worsened. He was
diagnosed at this time with an inferior wall STEMI due to late in-stent thrombosis and restenosis of his
right coronary artery and underwent successful revascularization. After step-down from the CCU, the
patient became acutely hypotensive and non-responsive. He was in cardiogenic shock due to a
ventricular tachycardia (VT). The VT was resistant to boluses of amiodarone, lidocaine, magnesium, and
external synchronized/unsynchronized shocks. An abnormality was noted in the patient’s EKG: a wide
complex tachycardia with a right bundle branch block morphology but left axis deviation. This finding
can be seen in a specific type of VT: idiopathic left VT, also known as verapamil sensitive VT or Belhassen
VT. With the patient in critical condition and not responding to treatments within the ACLS algorithm,
the decision was made to push verapamil. The VT immediately broke back into normal sinus rhythm
with resolution of the patient’s hypotension. A similar episode was rapidly treated with verapamil with
an identical response. Due to the significant hemodynamic instability during these episodes, he was
never able to pursue possible ablation. He was maintained on oral verapamil without further episodes.
DISCUSSION: Idiopathic left VT became known as Belhassen VT after Dr. Bellhassen reported the
termination of the arrhythmia with verapamil in 1979. This also why it is sometimes called verapamil
sensitive VT. This arrhythmia is historically seen in young healthy males with normal hearts complaining
of recurrent palpitations. This patient had never previously experienced palpitations or had a history of
arrhythmias. The subtle finding of a right bundle branch block morphology coupled with a left axis
deviation suggested that this may not be as simple as scar-mediated VT. Our theory was somewhat
confirmed given the patient’s immediate response to intravenous verapamil. The clinical dilemma
highlighted here revolves around the decision to push verapamil in a severely hypotensive patient due
to a VT. If this were another atypical cause for a wide complex tachycardia (ie a supraventricular
tachycardia with aberrancy) instead of scar induced VT or Belhassen VT, the treatment given could have
blocked the AV node and resulted in acute worsening of the tachycardia and hypotension as conduction
was shunted through an accessory pathway.
[Date]
CONCLUSIONS: Belhassen VT is typically seen in males with no cardiac disease presenting with recurrent
palpitations. It was potentially identified in a post STEMI patient with severe CAD presenting with acute
cardiogenic shock. This atypical presentation highlights the importance of utilizing ACLS algorithms when
responding to cardiac events while also considering atypical causes.
125
DISTRICT OF COLUMBIA POSTER FINALIST - CLINICAL VIGNETTE Myat Soe, MBBS
An Illusion for Pancreatic Cancer: Autoimmune Pancreatitis (AIP)
First Author: Myat Soe, MBBS Other authors: Manash Das, MD; Linda Green, MD
Introduction: Autoimmune pancreatitis (AIP) is a recently emerged entity of chronic pancreatitis of
autoimmune origin, first recognized by Sarles et al in 1961 as an idiopathic pancreatitis with obstructive
jaundice and hypergammaglobulinemia, with the term ‘AIP” first described by Yoshida et al in 1995. If
not carefully evaluated and not aware of the existence of this entity of pancreatitis, it can be
misdiagnosed as pancreatic cancer, leading to unnecessary pancreatic resection as AIP usually presents
as pancreatic mass with vague abdominal symptoms and weight loss.
Case Description: We present a case of AIP in a 77 years old African American man presenting with
vague upper abdominal pain, vomiting, significant weight loss, and new onset diabetes mellitus over 3
months period. Physical exam was unremarkable except for mild upper abdominal tenderness and
progressive weight loss. Laboratory evaluation revealed mild anemia, and mild conjugated
hyperbilirubinemia with elevated lipase and alkaline phosphatase. CT/MRI of abdomen and endoscopic
ultrasound revealed hypodense mass in the pancreatic head with main pancreatic duct dilatation and
bile duct stricture. ERCP showed distal common bile duct stricture and pancreatic stent was placed.
Given the constellation of these clinical features and data, pancreatic cancer was considered as the most
possible diagnosis. However, fine needle aspiration biopsies done for 2 times via endoscopic ultrasound
were negative for dysplasia and malignancy, but showed inflammatory infiltrates in glandular tissues. Ca
19-9 level and IgG4 level were within normal limit. Considering AIP as a possibility, the patient was
started on steroid trial, which he responded well. He had symptoms relief, better control of diabetes,
weight gain and complete resolution of pancreatic mass and bile duct stricture at the end of 6 months of
steroid treatment.
[Date]
Discussion: In summary, this case illustrates the existence of this new entity of chronic pancreatitis,
which can mimic pancreatic cancer, and importance of systematic evaluation of pancreatic mass with
timely expert consultation. Learning from this clinical vignette, AIP is an important differential diagnosis
to consider for pancreatic mass, in addition to pancreatic malignancy. Recently, it is classified as type 1lymphoplasmacytic sclerosing pancreatitis (LPSP) and type 2- idiopathic duct centric pancreatitis (IDCP).
Clinically, type 1 AIP appears to be pancreatic manifestation of systemic IgG4 related disease whereas
type 2 AIP does not have systemic involvement, as seen in our case. Both types may present as
pancreatic mass with obstructive jaundice, vague upper abdominal pain and weight loss, which can be
mistaken for pancreatic cancer. With International Consensus Diagnostic Criteria (ICDC), the incidence of
AIP has risen in the last few years and it is being increasingly recognized in Western population.
Improved diagnostic criteria (ICDC), advance in EUS guided FNA biopsy and steroid responsiveness
provide accurate and timely diagnosis of AIP and differentiate it from pancreatic cancer.
126
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Vivek Choksi, MD
Eosinophilic Polymyositis: A rare cause of severe rhabdomyolysis in a 22-year -old
female
First Author: Vivek Choksi1, Andrew Chu1, Ayesha Farooq1, Dhruti Mankodi1, Elana Oberstein11MD,
Aventura Hospital and Medical Center Internal Medicine Residency
Introduction: Eosinophilic myositis (EM) is an inflammatory myopathy characterized by the presence of
eosinophilic infiltrates in muscle, along with potential involvement of cardiac and central nervous
systems. We describe the case of a young patient with rhabdomyolysis, which we believed was caused
by eosinophilic polymyositis.
Case Presentation: A 22-year-old African American female with no past medical history presented to
the emergency department with complains progressive generalized diffuse muscle aches for
weeks. She denied recent illness, trauma, heavy physical exertion, excessive heat exposure, drug/
herbal medication usage, or medical or family history of autoimmune diseases. Examination of the
extremities revealed diffuse muscle tenderness on palpation with limited range of motion secondary to
muscle pain. Laboratory findings demonstrated no leukocytosis, but the percent of eosinophils was
elevated with absolute eosinophilia. Other significant laboratory findings were severely high creatine
phosphokinase (CPK) and transaminases. Patient was admitted for severe rhabdomyolysis requiring
aggressive IV fluid hydration. Work up for parasitic infections, systemic autoimmune diseases,
endocrine disorders, hematological diseases, and hypereosinophilic syndromes were ruled out. Muscle
biopsy showed widespread eosinophilic infiltrate consistent with eosinophilic polymyositis as well as
numerous plasma cells. The patient was started on high dose systemic corticosteroid. Her symptoms
gradually improved within 5 days. The absolute eosinophil count and CPK trended down, and patient
was discharged 4 weeks after hospitalization.
[Date]
Discussion: This case illustrates a systematic work up of rhabdomyolysis in the presence of peripheral
eosinophilia. Many differentials of eosinophilic myositis must be ruled out before establishing diagnosis
of idiopathic EM. Within idiopathic EM, defining different clinical presentations and muscle biopsy
results are required to conclude the diagnosis of Eosinophilic Polymyositis. To our knowledge, ours is the
first case report documenting severe rhabdomyolysis without other organ involvement, due to
eosinophilic polymyositis. EM is a relatively rare and understudied clinical entity, with no definitive
guidelines for treatment. The present case reports an unusual presentation of EM and successful
resolution with high dose corticosteroid therapy.
127
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Alexandra Gomez Arteaga, MD
Primary bone marrow gray zone lymphoma presenting with leukemic phase and
profound thrombocytopenia
First Author: ALEXANDRA GOMEZ ARTEAGA, MD Second Author: LUIS SANCHEZ, MD Third Author:
AUGUSTIN PIMENTEL,MD
Despite the involvement of the bone marrow in systemic lymphoma is a common event; Primary Bone
Marrow Lymphoma (PBML) is an extremely rare presentation with unclear clinicopathological diagnostic
criteria and prognosis.
Case Description: A 57-year-old man with history of DM and HTN, presented with 10-day history of back
pain, fatigue, diaphoresis, and 1 day of gingival bleeding and melena. He denied fever or
lymphadenopathy but he endorsed a 20 lb weight loss in the past 5 months. Physical exam revealed an
ill appearing, middle age Hispanic male with evidence of a diffuse petechial rash. He had no palpable
lymphadenopathy nor hepatosplenomegaly. Labwork revealed a WBC 8.7 x103/mcL, Hb 13.8 gr/dl,
platelets of 7,000/mcL. BMP was unremarkable but LDH was significantly elevated at 12,900 units/L. His
calcium and phosphorus were normal and uric Acid was elevated at 6.3mg/dL. HIV testing was negative.
Peripheral blood smear showed circulating immature looking lymphocytes , few tear drop cells and
markedly decreased platelets. Bone Marrow biopsy revealed extensive involvement by a high-grade B
cell lymphoma, unclassifiable (B-UCL), with features intermediate between diffuse large B cell
lymphoma (DLBCL) and Burkitt lymphoma. Immunohistochemistry showed that cells were positive for
CD20 and CD10 and negative for CD3, CD5, cyclin D1, CD34, TdT, and CD30. KI67 proliferation was 95%
and c-MYC was positive in >90% of tumor cell nuclei. Molecular studies using FISH panel was positive for
BCL-2 gene translocation t(14;18), but negative for BCL-6 and C-MYC rearrangements. CT scans of the
chest, abdomen and pelvis did not revealed enlarged lymph nodes or splenomegaly. CNS evaluation was
negative for leptomeningeal involvement. IPI was high-intermediate risk. Patient was started on DoseAdjusted EPOCH regimen, and following first cycle of treatment his constitutional manifestations
improved and the platelet count normalized. BM biopsy after 3rd cycle of treatment showed no
evidence of residual lymphoma consistent with a complete remission.
[Date]
Discussion: Lymphoma exclusively confined to the bone marrow with no lymphadenopathy or other
extranodal involvement has been reported in less than 20 case series/reports in the last 5 decades(1).
Martinez reported 21 cases from review of 12 institutions over a 25 year period which comprised 15
DLBCL, 4 Follicular, and 2 peripheral T-cell lymphomas (2). No other cases were found of B-UCL type
PBML. B-UCL is an aggressive lymphoma with the majority of patients presenting with advanced-stage
disease and high IPI scores. About 50% of the cases harbor a MYC translocation including 32% with
double hit rearrangements. Perry reported a median OS of 9 months and 5-year OS of 30% (3). Although
therapy is not standardized, response to R-CHOP is poor; therefore an intensive therapy approach is
advised in hope for improved outcomes (4).
128
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Brittany McCreery, MD
A CASE OF VANISHING PLEURAL EFFUSION
First Author: Brittany McCreery, MD Second Author: Rumi Khan, MD
CASE: A 53 year old male injection drug abuser with history of cirrhosis and CKD presented to the
emergency department with left arm redness and swelling. Blood cultures were obtained and empiric
antibiotics for presumptive cellulitis were started. Within two hours of presentation the patient
developed new symptoms of dyspnea and was found to be hypoxemic. Stat chest x-ray revealed
bilateral perihilar patchy infiltrates and right-sided effusion. CT thorax confirmed a large right pleural
effusion, no pulmonary emboli. Echocardiogram showed EF of 55% and normal valves. When a drug
screen returned positive for cocaine and opiates, upon further questioning, he admitted using heroin
the morning of presentation. Within 24 hours, his dyspnea resolved and he was successfully weaned off
supplemental oxygen. No diuretics were given. A follow up x-ray showed dramatic improvement of the
effusion and infiltrates. Cultures remained negative. He was discharged home with oral antibiotics.
BACKGROUND: According to the National Institute of Drug Abuse, 4.2 million Americans have used
heroin at least once, with the number of users doubling between 2007 and 2012. There was an
estimated 213,118 ED visits for heroin-related complications in 2009 alone. Heroin overdose is
manifested by a triad of altered mental status, miosis, and decreased respiratory drive. Hospitalization
occurs in 3-7% of cases, typically for prolonged respiratory depression, altered mental status, or noncardiogenic pulmonary edema (NCPE). NCPE in heroin overdose frequently presents within 2 hours of
use. Clinical findings include rales, frothy sputum, and hypoxia. Chest radiograph suggests bilateral
infiltrates, though unilateral and lobar infiltrates have been reported. Pathophysiology of heroin-related
NCPE is unclear. One proposed mechanism is opiate-mediated release of histamine in the lung
parenchyma increasing lymphatic flow and capillary permeability leading to edema. Recent case series
found NCPE rates of 2.1%- 10% in heroin overdose visits. NCPE commonly resolves in 24-36 hours with
supportive care, while a minority require intubation. Despite the favorable prognosis, NCPE occurs near
universally in fatal heroin overdoses.
[Date]
DISCUSSION: NCPE with infiltrates on chest x-ray has been previously described in presentations of
heroin overdose. In this case, however, the patient’s dominant radiological finding was pleural effusion.
The timing of onset and resolution fits the characteristic pattern of heroin overdose. The patient was
also cocaine positive, but available literature that describes cocaine induced pleural effusion shares
concomitant pericardial effusion and resolution of the effusion occurs over weeks. Normal
echocardiogram and negative cultures excluded alternative diagnoses such as heart failure and
pneumonia. This case appears to uniquely identify rapidly resolving pleural effusion as a complication of
heroin overdose and suggests this manifestation should be added to the spectrum of pulmonary
pathology associated with heroin overdose.
129
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Jordan C Ray, MD
Chemical Mediastinitis and Pericarditis Secondary to large Pancreaticopleuralmediastinal Fistula
First Author: Jordan C Ray, MD, Jason Prater M.D., Jose Melendez Rosado M.D., Brian P. Shapiro M.D.
Introduction: Pancreaticopleural fistulas are an uncommon complication of chronic pancreatitis and are
increasingly becoming more recognized. Commonly a result of disruption of the pancreatic duct
pancreaticopleural fistulas can lead to chemical inflammation resulting in pericarditis, mediastinitis and
pleuritis.
Case presentation: A 35-year-old male presented with one week of substernal chest and epigastric pain
with radiation to his back, and shortness of breath. A healthy male with past medical history only noted
for extensive alcohol abuse, the patient noted his chest pain worsened with inspiration, and lying flat on
his back. Basic laboratory studies were obtained noting normal lipase and liver functions. Initial
computed tomography of his chest revealed fluid collection in the posterior mediastinum with
additional collection around the aorta as well as a loculated right pleural effusion. Magnetic Resonance
(MR) imaging was obtained to further define the mediastinal fluid collection which revealed a very large
caliber fistula arising from the pancreatic duct at the junction of the body and tail tracking
posterosuperiorly to pass through the esophageal hiatus, directly abutting the posterior aspect of the
pericardium, which appeared thickened and extremely hyper-enhancing, consistent with pericarditis. A
complex right moderate loculated pleural effusion was also noted on MR. Thoracocentesis was
performed on the right pleural effusion and was shown to have elevated amylase consistent with a
pancreaticopleural fistula resulting in mediastinitis and pericarditis. The patient was initially treated
medically with pleural drains and octreotide. However, rapid accumulation of pleural effusions and
complex loculations prevented complete nonsurgical resolution. The patient was treated with surgical
drainage of the loculated pleural effusions with pleural decortication and continued chest tube drainage
for several weeks. Attempts to close the fistula from the pancreatic duct through endoscopic retrograde
pancreatoduodenography were unsuccessful as the proximal pancreatic duct was atretic and closed.
After removal of chest tubes repeat imaging showed improvement of fluid collection. Chest radiographs
at 6 months continued to show resolved pleural effusions.
[Date]
Discussion: Acute mediastinitis secondary to pancreaticopleural fistula has been infrequently described
in the medical literature. Commonly, mediastinitis is a result of tracking oral pharyngeal infection,
surgical complications or esophageal rupture. However, in rare cases, it can result from chemical
inflammation from pancreatic enzymes. Pancreaticopleural fistulas result most commonly from alcoholic
chronic pancreatitis. Treatment of fistulas commonly requires drainage of the fluid collections and
potentially surgical closure of fistulizing pathways.
130
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Jordan C Ray, MD
Immune Reconstitution Syndrome in a Patient with Suspected Rheumatoid
Arthritis Masking Late Onset Whipple’s Disease
Jordan C. Ray M.D.; Hilary Steele M.D.; Paul Cho; Jason T. Lewis, M.D.; Archana Roy, MD; Lisa Brumble
M.D.
Introduction: Late onset Whipple’s Disease is extremely rare with a reported incidence of
approximately 30 cases per year. Whipple’s classic presentation of migratory arthralgias, diarrhea and
abdominal pain most commonly affects middle aged males of European descent. Early on Whipple’s
disease can go misdiagnosed. Late in the disease patients often present with continued joint and
abdominal pain, significant weight loss, profound diarrhea and vitamin deficiencies. On occasion, an
Immune reconstitution syndrome can present on initiation of treatment. Its high fevers, joint pain and
hypotension can easily be confused with sepsis.
Case Presentation: A 55 year old female presented to an outside institution with dyspnea on exertion
and persistent diarrhea. Prior to admission the patient had a past history of migratory arthralgias for
approximately 15 years and had been on a myriad of biological and disease modifying agents for
suspected Rheumatoid arthritis without relief of her symptoms. Initial evaluation revealed a 40 pound
weight loss over 6 months, non ischemic cardiomyopathy and iron deficiency anemia. Celiac sprue was
suspected and the patient underwent endoscopy with small bowel biopsies which showed foamy
macrophages with Whipple bacillus strains stained with PAS stain. The patient was diagnosed Whipple’s
disease and underwent initial treatment with ceftriaxone. Approximately four hours after initial
treatment the patient presented with fever, chest pain, diffuse arthralgias, rash and hypotension. Sepsis
was suspected and the patient underwent invasive monitoring, broad spectrum antibiotics and the use
of vasopressor medications. This syndrome persisted despite continued treatment with intravenous
antibiotics. With a concern for sepsis versus a drug reaction the patient was transferred to a local
tertiary center for further management. Immune reconstitution reaction was suspected. Multiple
biopsies of skin lesions reviled erythema nodosum- like lesions and septal panniculitis with PCR positive
for Tropheryma Whipplei. The patient completed a course of 14 days of intravenous antibiotics with a
gradual decline in her immune reconstitution syndrome. She was discharged with follow up and a 1 year
course of trimethoprim-sulfamethoxazole.
[Date]
Discussion: Whipple’s disease is a rare condition with vague symptoms which can easily mimic other
arthritic conditions. Vitamin deficiencies and their sequela including heart failure can occur as
malabsorption is a common late manifestation. In patients who have received previous
immunosuppressive therapies the potential for immune reconstitution syndrome increases. Immune
reconstitution can present with erythema nodosum and a severe inflammatory syndrome that can
mimic septic shock. The treatment of Whipple’s disease is prolonged involving both intravenous and oral
antibiotics for a total course of close to one year.
131
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Debjit Saha, MD
Foix- Alajouanine syndrome: A rare and treatable cause of paraplegia
First Author: Debjit Saha, MD Pooja Pundhir, M.D. Hany Elmahdy, M.D. John Chaloupka, M.D.
Spinal dural arteriovenous fistulas (SDAFs), also known as Foix- Alajouanine syndrome, are a rare and
commonly under-diagnosed cause of myelopathy. It usually presents as a myelopathy slowly progressing
to paraplegia, commonly found in men in their fifth decade of life.
A 59-year-old male with a past medical history of hypertension, gastrectomy secondary to vitamin B12
deficiency and alcohol dependence, presented to the emergency room with progressive bilateral lower
extremity weakness and claudication that started one week prior. This gradually progressed proximally
limiting his ability to stand and sit, resulting in multiple falls. He also noticed new lower extremity distal
paresthesias in the last day. He also had an episode of spontaneously resolving non-bloody diarrhea two
weeks prior while visiting Ecuador. Examination was remarkable for morbid obesity, lower extremity
paraparesis, 3/5 muscle strength distally and 2/5 in hip flexors, worse on the left. Bilateral patellar and
Achilles reflexes were absent, as well as Babinski’s. There was no evidence of saddle anesthesia and
rectal tone was intact. Initial differentials were Guillain-Barre Syndrome, B12-deficiency related
neuropathy or spinal canal stenosis. MRI revealed moderate L3/L4 spinal canal stenosis with bilateral
foraminal narrowing with suspicion for flow voids in the left thoracic spinal cord vasculature suggestive
of possible dural AV fistula (DAVF). A subsequent diagnostic spinal angiogram confirmed a left T11 DAVF.
A transarterial embolization of the AV fistula was performed by the neuro-interventional radiologist. The
patient recovered remarkably with resolution of weakness and paresthesias the next day.
[Date]
Our patient presented with progressive myeloradiculopathy, which was diagnosed as SDAF and treated
successfully. The initial symptoms of this disease entity usually consist of gait disturbances, numbness,
paresthesias and intermittent radicular pain mimicking peripheral nerve lesions. This wide range of
symptoms often make the diagnosis delayed resulting in irreversible paraparesis with sensory and
sphincter disturbance. SDAF usually consists of an arteriovenous shunt between a branch of a dural
artery and a medullary vein resulting in coronal venous plexus hypertension with subsequent decreased
cord perfusion and progressive congestive myelopathy. MRI with contrast enhanced angiography (MRA)
has 80-90 % sensitivity; it commonly displays a non-specific hyperintense T2 signal. CT myelography can
be done alternatively, which may demonstrate the serpentine vessels within the intradural space. These
studies can guide the spinal angiogram, which is the gold standard diagnostic test and required for
therapeutic intervention. Occlusion of the fistula by surgery or endovascular embolization is helpful in
stabilizing or curing the neurological deficits. Our case exemplifies that a high index of suspicion with
prompt diagnosis and appropriate management can stop the progression to irreversible neurologic
impairments in patients with SDAF.
132
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Wassim Samra, MD
A new diagnosis of Hemoglobin SC Disease saves a woman’s life
First Author: Wassim Samra, MD
A 52 yo Black woman with a medical history only significant for hypertension presented to the ED due to
acute onset right sided pleuritic chest pain associated with shortness of breath. In the ED, CT Angiogram
of the chest showed subsegmental pulmonary artery filling defects consistent with PE and no
consolidation. Lower extremity dopplers were negative for DVT. Within 48 hours, patient’s dyspnea and
chest pain worsened. She developed a fever and her chest xray showed new infiltrates. Her labs on
admission showed a hemolytic anemia. Her CT revealed a small, calcified spleen. These findings led to
the suspicion of an underlying, undiagnosed hemoglobinopathy. She denied any known history of
anemia, sickle cell crisis, or family history of sickle cell diseases. Despite treatment with broad spectrum
antibiotics for pneumonia, her respiratory status continued to deteriorate. Her hemoglobin
electrophoresis panel came back with a Hgb S of 43.8%, Hgb C of 43.8 % and Hgb F of 12.4%, consistent
with Hgb SC disease. At this point the diagnosis of acute chest syndrome was made and she was quickly
started on exchange transfusion. She was also continued on treatment with antibiotics, anticoagulation,
aggressive hydration, and supplemental oxygen. Within 2 days, her respiratory status improved and she
was no longer requiring oxygen.
[Date]
Discussion: Acute chest syndrome (ACS) is a known complication and a leading cause of death for
patients with sickle cell syndromes. However, the incidence of ACS in patients with HbSC is significantly
less than that seen in HbSS. In this particular case, the investigation of the unexplained anemia and the
calcified spleen led us to the new diagnosis of hemoglobin SC disease. Fortunately, with this knowledge,
the diagnosis of ACS was made which led to appropriate treatment of exchange transfusion, preventing
further deterioration and death. This case is unique because this patient’s initial presentation of a crisis
was acute chest syndrome, rather than the typical presentation of a painful crisis. In retrospect, the
pulmonary artery filling defects were realized to be in-situ thrombi of sickled cells rather than emboli.
This case illustrates the importance of considering hemoglobinopathy and acute chest syndrome,
especially in African American patients, presenting with hemolytic anemia and acute respiratory
symptoms, or findings of pulmonary embolism.
133
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Sam Thomas, MD
A Rare Case of Goblet Cell Carcinoid Tumor Presenting as Small Bowel Obstruction
First Author: Sam Thomas, MD Preceptor: Dr. Lara Zuberi
A 51 year old male presented to our hospital with a three day history of colicky right lower quadrant
abdominal pain with nausea and vomiting. Vitals were stable, and physical exam showed diffuse
abdominal tenderness with increased severity localized to the right lower quadrant. A CT scan of the
abdomen and pelvis revealed multiple dilated and fluid filled loops of small bowel with transition point
involving the terminal ileum. It showed circumferential thickening with no definitive mass seen,
suggestive of terminal ileitis.
Symptoms did not respond with aggressive non-operative management, therefore the patient was taken
to the operating room for exploratory laparotomy. A 5-cm cecal mass diffusely involving the appendix
was discovered with extension into the wall of the cecum and ileum. A right hemicolectomy with small
bowel resection and lymph node resection was then performed. Immunohistochemical stains of the
mass were positive for chromogranin, synaptophysin and CK20 which confirmed the diagnosis of poorly
differentiated goblet cell carcinoid tumor.
The tumor penetrated into the surface of the visceral peritoneum and directly invaded the cecum and
ileum with lymphovascular invasion. Twenty seven lymph nodes were examined with six being involved.
By post-op day three, the patient had return of bowel function and began to tolerate a diet. The patient
was followed up and to date the post operative period has been uneventful.
[Date]
Goblet cell carcinoid or adenocarcinoid is a rare variant of appendiceal carcinoid with mixed endocrine
and exocrine features. They often present with symptoms of an inflamed appendix, which makes this
case especially rare given the extensive tumor extension which resulted in a small bowel obstruction.
They rarely present with serotonin syndrome. Goblet cell carcinoids are treated with right-sided
hemicolectomy and lymphadenectomy and in many cases chemotherapy can be utilized. Goblet cell
carcinoids have a 10-year survival rate of approximately 60%.
134
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Prakhar Vijayvargiya, MD
Neurocysticercosis presenting as Chronic Relapsing Aseptic Meningitis
First Author: Prakhar Vijayvargiya Second Author: Larry M. Bush Third Author: Maria T. Perez
Neurocysticercosis with chronic relapsing aseptic meningitis is a rare clinical entity. We present a case of
neurocysticercosis that presented in such a relapsing fashion that necessitated craniotomy to eventually
make a diagnosis. A 60 year old female with no significant past medical history presented in the late
winter months complaining of acute onset of severe headache of two days duration. She described the
headache as diffuse, constant and the worst that she has ever had. She mentioned travel to Central and
South America in the preceding few years. Rest of history and physical examination was unremarkable.
Laboratory tests were within normal limits. CT scan prior to lumbar puncture was normal. Spinal fluid
analysis was suggestive of pleocytosis (78% lymphocytes) with negative cytologic and microbiological
studies. MRI of brain was interpreted as normal. Her headache improved on symptomatic treatment and
she remained well until 14 months later when she presented with similar symptoms. During this
hospitalization, MRI of brain was found to have prominent leptomeningeal enhancement along the
sylvian fissure and suprasellar cistern. Spectroscopy did not demonstrate evidence of tumor spectra.
Once again her symptoms fully resolved with analgesics and empirical antibiotics. However, she
presented for a third time six weeks later with exact same clinical scenario. Follow up MRI was felt to
now have worsening of meningeal thickening. She underwent a craniotomy with biopsy of the affected
area. Surprisingly, on histologic examination a parasite consistent with Taenia solium was seen. She
received a one month treatment of albendazole (400 mg BID) along with a tapering course of
dexamethasone and has been clinically well for over a follow up period of 8 months. The cysticerci of
pork tapeworm (Taenia solium) may rarely involve the ventricles or subarachnoid space
(extraparenchymal neurocysticercosis).
[Date]
When it involves the meninges, CSF analysis mirrors tuberculosis or fungal meningitis with lymphocytic
pleocytosis. Diagnosis relies on astute clinical acumen as, depending on the stage of the infection,
imaging may only demonstrate subtle abnormalities. Ring enhancement, edema and calcification may
be seen only in advanced cases . Our patient's presentation was peculiar in that the symptomatic
meningitis episodes were separated by long periods of feeling well. Only a few cases have been
documented in the literature with chronic relapsing meningitis secondary to neurocysticercosis. High
index of clinical suspicion is therefore required to make an diagnosis. This case also emphasizes the need
for early tissue diagnosis in instances where the diagnosis is otherwise elusive.
135
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Danlu Wang, DO
Myeloid Sarcoma Mimicking Acute Appendicitis as the Initial Presentation of Acute
Promyelocytic Leukemia
First Author: Danlu Wang D.O. Second Authors: Marvin Lopez M.D. Second Author: Eduardo Rodriguez
M.D. Attending: Andrew Fischer M.D.
Extramedullary involvement in acute promyelocytic leukemia (APL) is a rare condition. Most reported
cases tend to involve the central nervous system or skin and less frequently other sites. Although
leukemic and lymphomatous infiltration of the gastrointestinal tract has been well document, the
involvement of the appendix in cases of APL is very limited. We present the case of a patient with
myeloid sarcoma (MS) of the appendix as initial presentation of APL.
A 43 year old female patient with no significant past medical history presents to the emergency room
complaining of persistent fevers, weakness and fatigue for the past two weeks with mild lower quadrant
abdominal pain for the past two days. Vital signs were significant for heart rate of 115 beats/minute and
temperature of 101.4 F. On physical examination, patient had pale conjunctiva, no lymphadenopathy
could be appreciated, lungs were clear to auscultation and abdomen was soft, non-distended, with mild
tenderness in the right lower quadrant without signs of peritoneal irritation. Initial laboratory results
were significant for hemoglobin of 6.8 g/dL, 2,000 white blood cells/uL with: 12% segmented, 3% bands,
40% lymphocytes, 4% monocytes, 4% metamyelocytes, 2% promyelocytes, 4% blasts, 20% other cells
and platelets of 3,000. Fibrin degradation products >20 mcg/ml and D-Dimer >35.2 mg/L FEU. CT of the
abdomen showed a thickened and hyperemic appendix without perforation or abscess, compatible with
acute appendicitis. Initial treatment consisted of transfusion of packed red blood cells, platelets and
initiation of broad-spectrum antibiotics. Once the patient was stabilized, she underwent bone marrow
biopsy and laparoscopic appendectomy, without complications. Subsequent bone marrow biopsy
revealed t(15:17) and (q22:12) mutations and reverse transcriptase-polymerase chain reaction (RT-PCR)
for PML-RARA demonstrated a long form fusion transcript consistent with the diagnosis of APL.
Appendix pathology relieved infiltration by leukemic blasts that co-expressed myeloperoxidase and
CD68, consistent with myeloid sarcoma of the appendix. The patient completed a course of ATRA,
daunorubicin and cytarabine. Repeat bone marrow biopsy demonstrated complete remission and the
patient was subsequently discharged home.
[Date]
The association of acute appendicitis in the setting of acute leukemia has been previously described
however documented cases of appendiceal involvement in APL are not common. To our knowledge this
is the first documented case of a patient with MS of the appendix mimicking acute appendicitis as the
first presentation of APL that underwent chemotherapy and was discharged with remission of the
disease. Leukemic infiltrate may have caused the inflammation of the appendix ultimately leading to the
presentation of acute appendicitis. MS can arise concurrently with, follow, or precede the diagnosis of
intramedullary acute myelogenous leukemia.
136
FLORIDA POSTER FINALIST - CLINICAL VIGNETTE Mohamad Zetir, MD
Intestinal Angioedema in the Setting of Angiotensin Receptor Blocker Use
First Author: Mohamad Zetir, MD Mary S. Hedges, M.D.
Intestinal angioedema is a rare cause of abdominal pain in patients, and the diagnosis is often missed.
The condition can be either hereditary or caused by the use of angiotensin converting enzyme inhibitors
(ACE-I) and even less commonly, angiotensin receptor blockers (ARB). Patient is a pleasant 27 year-old
woman with a past medical history of hypertension who was admitted to our hospital due to abdominal
pain.
The Patient described the pain as an abrupt stabbing-like sensation in her mid-abdomen, which spread
diffusely. This was followed by an episode of profuse non-bloody diarrhea. Other associated symptoms
included nausea and an episode of non-bloody vomiting. Patient denied fevers, chills, or family history
of inflammatory bowel disease. Patient experienced similar symptoms in the past when she was placed
on an Angiotensin receptor blocker due to hypertension. Patient was initially placed on an ACE-I which
was discontinued due to cough. Prior to her admission at our hospital, patient presented to an outside
hospital due to similar symptoms and was discharged on a short course of Flagyl/Cefdinir with no
improvement in symptoms. Patient was later re-admitted to the outside hospital, and CT of the
abdomen and pelvis showed dilated bowel loops and edematous bowel walls. Patient underwent an
EGD as well as a colonoscopy with biopsies, which was reportedly negative for inflammatory bowel
disease. Patient was ultimately discharged home with the diagnosis of infectious enteritis and received a
7-day course of meropenem through a PICC. Patient was admitted to our institution due to recurrence
of symptoms. During the admission, an extensive chart review of outside records, as well as an extensive
medication review was performed. The ARB was discontinued with a presumed diagnosis of Intestinal
angioedema and patient reported improvement in symptoms.
[Date]
A follow up two months after discharge confirms cessation of symptoms. Intestinal angioedema can
present as abdominal pain, with associated nausea, vomiting and diarrhea. Abdominal CT or ultrasound
can be used to detect abdominal wall edema. Intestinal angioedema is seen in patients on ACE-I and in
patients with C1 inhibitor deficiency. It is a rare diagnosis that is often misdiagnosed as other abdominal
etiologies such as gastroenteritis. Angiotensin receptor blockers rarely cause angioedema, with
intestinal angioedema being even rarer. It is vital to make this diagnosis early to avoid unnecessary
testing and treatments.
137
GEORGIA POSTER FINALIST - CLINICAL VIGNETTE Daisy Azana, MD
Hemolytic Uremic Syndrome, a rare manifestation of Clostridium Difficile colitis
First Author: Daisy Azana, MD Zina Abbas, MD Riyadh Al-Rubaye, MD Nomi Traub, MD
Hemolytic Uremic Syndrome (HUS), characterized by a triad of hemolytic anemia, thrombocytopenia,
and acute renal failure, usually occurs in children, often following a diarrheal illness. We report a case of
HUS in an adult, associated with colitis due to Clostridium difficile.
A 32 year old Hispanic female with a history of IV drug use presented with a 3 day history of fever,
bloody diarrhea and abdominal pain. She denied recent antibiotic use, sick contacts, or travel. She
appeared acutely ill with a temperature of 36.2°C, heart rate of 110-142, and blood pressure of 94/70
mm Hg. Her abdomen was distended with moderate diffuse tenderness.
Initial laboratory data showed a hematocrit of 41.2%, WBC of 16 x 103/µL, platelet count of 314 x 109/L,
creatinine of 0.9 mg/dL, and PT /PTT within normal limits. CT scan of the abdomen and pelvis revealed
severe colitis from the cecum to the descending colon. Empiric antibiotic therapy (IV ciprofloxacin and
metronidazole) was initiated for treatment of infectious colitis. Stool from the first day of admission
was positive for Clostridium difficile toxin by enzyme immunoassay; cultures for E coli O157:H7,
Salmonella and Shigella were negative. Oral vancomycin and metronidazole were substituted for the
antibiotic regimen.
During hospitalization, the patient developed microangiopathic hemolytic anemia, thrombocytopenia,
and renal failure. Laboratory findings included a hematocrit level of 17.2%, with a reticulocyte count of
4%, a platelet nadir of 31 x 109/L, and lactate dehydrogenase (LDH) of 1414 U/L. Peripheral blood smear
revealed schistocytes. The patient's creatinine peaked at 5.5 mg/dL. A renal biopsy displaying
thrombotic microangiopathy supported our presumptive diagnosis of HUS associated with Clostridium
difficile colitis.
This case demonstrates a rare association between Clostridium difficile colitis and HUS in the adult
population. With the rising incidence of Clostridium difficile colitis, physicians may encounter unusual
manifestations of this common illness.
[Date]
The patient underwent plasmapheresis, hemodialysis, and continued on oral vancomycin and
metronidazole for a total of 21 days. The patient received 13 plasmapheresis sessions, followed by 2
doses of rituximab due to slow improvement of thrombocytopenia. At discharge, the patient's
creatinine level was 1.7 mg/dL, platelet count was 147 x 109/L, hematocrit was 25.2%, and LDH was 241
U/L. Three prior adult cases of HUS associated with Clostridium difficile colitis have been reported. All
were women who survived without renal or neurologic deficits. Adult cases seem to have a better
prognosis compared to pediatric cases. The pathogenesis of HUS associated with Clostridium difficile
colitis is unclear. Animal experiments have demonstrated that Clostridium difficile toxin A induces
endothelial cell dysfunction in mesenteric venules, potentially leading to a disruption in the
mucosa. Through this type of breach, Clostridium difficile toxins may directly damage renal
microvasculature. This association needs further investigation.
138
GEORGIA POSTER FINALIST - CLINICAL VIGNETTE Mohammed Hasan Khan, MD
Gordonia: Master of Disguise, Cause of Infections
First Author: Mohammed Hasan Khan, MD Abhishek Garg MD Tarun Kukkadapu MD Amudhan
Jyothidasan MD
Gordonia spp are gram positive coryneform bacilli which are difficult to identify and rarely implicated in
infections in both immunocompetent and immunocompromised humans. They were previously
classified as Rhodococcus spp and continue to be misunderstood as such. They have been identified as
causative agents of catheter related blood stream infections [CRBSI], brain abscess, endocarditis and
cutaneous infections. We present a case of pacemaker pocket infection caused by Gordonia bronchialis
one of five gordonia species implicated in human infections.
An 81 year old female presented with syncope found to be due to sick sinus syndrome and a permanent
pacemaker was implanted uneventfully. Five weeks after implantation she started developing fevers and
pain and erythema at the surgical site following which she returned to the hospital, cultures were drawn
and she was started empirically on levofloxacin. The organism was a gram positive coryneform bacillus
initially identified as rhodococcus but cultures later grew Gordonia bronchialis susceptible to
fluoroquinolones, cephalosporins, sulfa based antibiotics and doxycycline. The device was removed and
she was treated with Bactrim to complete the course followed by re-implantation of the device and was
discharged home on doxycycline for ten more days.
[Date]
Five gordonia spp implicated in infections are Gordonia terrae, Gordonia bronchialis, Gordonia
polyisoprenivorans, Gordonia sputi and Gordonia otitidis. These organisms have been implicated in
CRBSI, endocarditis, brain abscess and cutaneous infections. Like all gram positive bacilli they are
difficult to identify and the use of HPLC is required to determine the genus level and
separate Gordonia from the related genera Dietzia, Corynebacterium, Rhodococcus and Tsukamurella.
This is important for appropriate identification of the organism and institution of appropriate antibiotics.
Our case highlights the importance of considering performing PCR-RFLP and HPLC to identify gordonia
spp. in cases of infection with gram positive bacilli to avoid confusion with morphologically similar
organisms. This also has practical implications as gordonia has been known to cause endocarditis which
could alter management with appropriate identification.
139
GEORGIA POSTER FINALIST - CLINICAL VIGNETTE CPT David Schmitt, MC USA
Hemoptysis in a Triathlete: A Case of Swimming Induced Pulmonary Edema
CPT David Schmitt, DO (Associate); MAJ Samuel Burkett, MD (Member); COL Michael Quinn, MD (FACP),
D.D. Eisenhower Army Medical Center
Introduction: Acute pulmonary edema, not associated with aspiration or a closed glottis, has been
described in swimmers and divers and has been termed Swimming Induced Pulmonary Edema
(SIPE). The exact pathophysiology of SIPE remains uncertain. This case illustrates a presentation of SIPE
in a healthy, male triathlete.
Case Presentation: A healthy, 57 year-old, active duty male developed acute dyspnea, productive
cough, and hemoptysis within minutes of starting the swimming portion of a triathlon in late
September. The patient reported taking aspirin 325mg daily and a white willow bark supplement
containing Salicin. In the Emergency Department, the patient’s symptoms had improved
significantly. His physical examination revealed bilateral rales and a normal cardiac examination. A
chest radiograph demonstrated increased central vascularity and a computed tomography pulmonary
angiography revealed scattered ground-glass opacities in an upper lung field distribution. Bronchoscopy
revealed alveolar hemorrhage, the presence of venous lakes, and bronchoalveolar lavage fluid was
negative for infection or malignancy. The patient’s symptoms resolved over the initial 24 hours.
[Date]
Discussion: Swimming-induced pulmonary edema (SIPE) is a syndrome whose pathophysiologic
characteristics have not been fully elucidated. Cold water immersion, coupled with an elevated cardiac
output, may expose regions of the capillary bed to high pressures that favor the extravasation of fluid by
hydrostatic forces and potential stress failure of the capillaries. Confounding factors in this patient’s
case were the use of antiplatelet medications and the presence of venous lakes on
bronchoscopy. Patients with SIPE present with dyspnea, cough, hypoxemia, and occasionally
hemoptysis. Physical examination and chest radiographs usually reveal evidence of pulmonary edema.
Treatment is symptomatic and conservative. Improvement and resolution of symptoms are usually
rapid, with radiographic normalization in 24 to 48 hours.
140
GEORGIA POSTER FINALIST - CLINICAL VIGNETTE Kelly D Schrapp, MD
A rare case of Moya Moya disease in an African American male
First Author: Kelly D Schrapp, MD
Introduction: Moyamoya is a chronic progressive cerebrovascular disease characterized by bilateral
stenosis of the arteries around the Circle of Willis with prominent arterial collateral circulation. We
describe a case of young male who presented with isolated right hand weakness which was diagnosed
with Moyamoya disease. The purpose of this case report is to draw attention to this disease, not as
familiar in Internal Medicine as in neurology.
Case Presentation: 40-year-old African American male with history of hypertension presented with
acute numbness and weakness of right hand of one day duration. He spontaneously regained some
mobility initially but same symptoms returned the next day associated with severe headache and
photophobia. Social and Family history were not significant. Patient’s blood pressure was 172/110
mmHg on admission. Physical examination was essentially benign except for decreased sensation and
strength of 1/5 in right hand. Right forearm and arm had normal strength and sensation. Rest of neuro
exam was normal. CBC, CMP, TSH, B12 were normal. ANA panel, ACE level, Sjogren AB, HIV, UDS, RF,
ESR, lyme disease AB, SPEP, SSA, SSB, RPR, P-ANCA, C-ANCA were all negative. CT head was negative.
CSF analysis including west nile were negative. MRI brain was done at this time which showed several
foci of restricted diffusion, encephalomalacia, gliosis were found in left posterior and anterior frontal
lobes compatible with acute to early subacute infarction. Angiography done showed attenuated and
irregular anterior greater than posterior circulation. No flow was found in either anterior cerebral artery.
Cervical, petrous, cavernous internal carotid arteries were patent but diminutive on the right.
Supraclinoid internal carotid arteries were narrowed thread-like, right more than left. Distal MCA
branches were narrow thread like with extensive collateral circulation. Vertebral arteries were patent,
with minimal irregularity in the distal right. The basilar artery demonstrated mild narrowing irregularity
in its mid and distal segments. The superior cerebellar and posterior cerebral arteries were patent. A
cerebral angiogram was done which confirmed Moya Moya disease.
[Date]
Discussion: Moyamoya disease is a progressive occlusion of cerebral arteries, particularly involving the
Circle of Willis and the arteries feeding it. The network of vascular collaterals developing bordering
stenotic vessels gives rise to the emergence of a “puff of smoke” (Moyamoya in Japanese) on
angiography. The stenoses are typically bilateral. However, unilateral involvement does not exclude the
disease. It was first described in Japan and mostly found in Japan and other Asian countries. It has been
found less frequently in Europe and North America. The occlusive lesions in the Circle of Willis rarely
progress in adult patients. Only 8 cases have been reported to display the progression of occlusive
lesions in adult patients with Moyamoya disease.
141
GEORGIA POSTER FINALIST - CLINICAL VIGNETTE Christopher J Walsh, MD
The Association Between Atrial Fibrillation and Sleep Apnea
Christopher Walsh, MD, Alan Zevallos, MD, Allen Tindol, MD, Department of Internal Medicine
Education, Memorial University Medical Center, Savannah, Georgia, Mercer University School of
Medicine, Savannah Campus
In patients with newly diagnosed atrial fibrillation (AF), physicians should investigate the possibility of
underlying sleep apnea, which predisposes to cardiac arrhythmias, including atrial fibrillation. Treatment of
underlying sleep apnea tends to prolong the period of normal sinus rhythm (NSR) following
electrocardioversion or catheter ablation.1 Conversely, following catheter ablation for AF, the existence of
underlying sleep apnea confers a 25% greater risk of AF recurrence.2 Though an association between AF and
sleep apnea appears to exist, causality remains uncertain, and the mechanism unclear.
A 61-year-old academic internist was making Saturday rounds with residents, when he experienced
palpitations. In the emergency department, he was found to be in AF with a ventricular rate of 140 beats per
minute. After receiving diltiazem, his systolic blood pressure dropped into the 70s, with heart rate in the 30s.
He was admitted for observation. Although his rate normalized with metoprolol, his rhythm remained AF.
Thyroid hormone, metabolic panel, blood count, cardiac enzymes, chest radiograph, and echocardiogram
were normal. He had no prior history of hypertension, AF, or other cardiac arrhythmias. Except for patent
foramen ovale (PFO), his past history was negative for heart conditions. He had no contributory family
medical history, did not smoke or drink, was not known to snore, and denied significant daytime sleepiness.
His body mass index (BMI) was normal at 23.7. His shirt neck size was 16.5 inches. Following a 3-week course
of apixaban, he underwent successful electrocardioversion. Unfortunately, he remained in sinus rhythm for
only 3 days, and afterward required metoprolol and digoxin for rate control. Though suggestive symptoms
were lacking, the patient’s cardiologist proposed the possibility of concomitant sleep-disordered breathing,
and the patient reluctantly underwent overnight polysomnography. The 7-hour study documented 65
obstructive apneas, 49 central apneas, 36 mixed apneas, and 14 hypopneas, for an apnea-hypopnea index
(AHI) of 23, denoting "moderate" sleep apnea. Subsequent overnight polysomnography documented the
efficacy of Adaptive Servo Ventilation (ASV) in overcoming the mixed and central components of the patient’s
sleep-disordered breathing, and the patient began nightly therapy. Shortly thereafter, the patient substituted
dronedarone for digoxin and metoprolol. A second elective electrocardioversion successfully restored NSR.
Approximately 8 months after his second electrocardioversion, the patient remains in NSR, without
occupational or lifestyle limitations.
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Reference 1 Kanagala R, Murali N, Friedman P, Ammash N, Gersh B, Ballman K, Shamsuzzaman A, and Somers V. Obstructive Sleep
Apnea and the Recurrence of Atrial Fibrillation. Circulation. 2003;107:2589-2594.
Reference 2 Ng C, Liu T, Shehata M, Stevens S, Chugh S, Wang X. Meta-Analysis of Obstructive Sleep Apnea as Predictor of Atrial
Fibrillation Recurrence After Catheter Ablation. American Journal of Cardiology. 2011;108, Issue 1:47-51.
Reference 3 Leung R, Huber M, Rogge T, Maimon N, Chiu K, Bradley T. Association Between Atrial Fibrillation and Central Sleep
Apnea. SLEEP. 2005;28(12):1543-1546.
Reference 4 Caples S, Somers V. Sleep-disordered breathing and atrial fibrillation. Prog Cardiovasc Dis. 2009;51:411–415.
[Date]
Sleep apnea causes hypoxemia, inflammation, sympathetic hyperactivity, and hypertension, and, along with
other factors, can lead to left atrial enlargement and eventual AF. Treatment of sleep apnea with continuous
positive airway pressure (CPAP) has beneficial effects on those factors. Therefore, the diagnosis of sleep
apnea (especially central sleep apnea3) should always be considered – and appropriate treatment attempted
– in the management of AF.4
142
HAWAII POSTER FINALIST - CLINICAL VIGNETTE Ittikorn Spanuchart, MD
Retrograde Cerebral Venous Air Embolism Secondary to Hepatic Portal Venous Gas
Ittikorn Spanuchart, Qi Jie Nicholas Leo, Aileen Tamura, Shane Wo, Brent Matsuda, Hiro Sung
Cerebral air embolism is a rare, yet potentially fatal condition. We present a case of retrograde cerebral
venous air emboli arising from hepatic portal venous gas secondary to mesenteric infarction.
A 69-year-old male with history of gastric amyloidosis, presented to the hospital with two days of fever
and lethargy. Upon arrival, he was found to be critically ill requiring emergent intubation and
subsequent transfer to the intensive care unit. Patient's abdomen was rigid and absent bowel sounds
were noted on physical examination. Despite aggressive fluid resuscitation, he required initiation of
norepinephrine. Empiric antibiotic coverage with piperacillin-tazobactam and vancomycin were chosen
for presumed septic shock. Pertinent laboratory tests revealed a WBC count of 24.5 with 28% bands,
elevated creatinine 0.9 (baseline 0.3), arterial pH 6.94, HCO3 11.8 and lactic acid level 10.8. CT scan of
the brain detected multiple foci of air in the right frontal, fronto-parietal, and left lateral frontal sulci
consistent with cerebral venous air emboli. Further imaging including CT scan of the abdomen and pelvis
revealed moderate thickening and dilatation of the small bowel with diffuse scattered intestinal
pneumatosis suggestive of mesenteric infarction with resultant extensive intrahepatic portal venous gas.
The patient was deemed a poor candidate for surgical intervention and died as a result of septic shock.
We believe the cerebral venous air emboli was a result of retrograde flow of air arising from the hepatic
venous gas ascending via the inferior and superior vena cava to the cerebral venous system.
[Date]
Paradoxical air embolism to the brain is less likely mechanism in this case due to the absence of air in
the cerebral arterial system. To our knowledge, there have been no reported cases of retrograde
cerebral venous air embolism arising from hepatic portal venous gas. The clinical significance and
prognosis in this setting requires further investigation.
143
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Adjoa Anyane-Yeboa, MD
A Case of Black Esophagus After PEA Arrest
Adjoa Anyane-Yeboa
Introduction: Esophageal necrosis or “black esophagus” is an extremely rare disorder of the esophagus
with only few cases described in the medical literature (1, 7). The pathogenesis of the disorder is
unknown; however, several investigators have postulated that an ischemic insult leading to esophageal
hypoperfusion may be a contributing factor (1, 3, 4). Patients often present with symptoms of acute
upper GI bleeding, with diagnostic endoscopy showing circumferential esophageal necrosis terminating
at the GE junction (1, 4). Here we present a case of esophageal necrosis in a patient after cardiac arrest.
Case: The patient is a 50-year-old man who presented with melena. Two weeks prior, the patient had
cadaveric renal transplant for end stage renal disease. Post-operative course was complicated by
cardiac arrest with pulseless electrical activity. The patient underwent 5 minutes of cardiopulmonary
resuscitation with return of spontaneous circulation. He was started on a cooling protocol, antibiotics
and vasopressors. He later developed large volume melena with hemoglobin drop from 8 to 6
grams. Subsequent upper GI endoscopy was significant for black discoloration and sloughing mucosa
from the mid-esophagus to the GE junction. The cardia, body and incisura of the stomach were
normal. Endoscopic findings were consistent with esophageal necrosis. Repeat endoscopy two
months later showed resolution of necrosis.
Discussion: Black esophagus is an extremely rare disorder of the esophagus. Risk factors for the
development of black esophagus include male sex and age older than 65 (5). It has been theorized that
the higher frequency of black esophagus in men is because men have a higher percentage of
atherosclerotic vascular disease and other comorbid illnesses that put them at increased risk for
development of ischemia (6, 8). Other risk factors include renal failure, malnutrition, hyperglycemia,
sepsis, malignancy, comorbid cardiovascular disease, and hypercoagulability (5).
Definitive diagnosis of black esophagus is made via upper endoscopy (1, 4). An endoscopic finding of
circumferentially black, necrotic esophageal mucosa with predominant involvement in the distal onethird is diagnostic (1, 4). With typical endoscopic findings, the diagnosis of black esophagus can be made
once ingestion of corrosive agents has been ruled out (1). Treatment is mainly supportive. Black
esophagus typically resolves with resolution of the underlying problem. Intravenous acid suppression,
most frequently with proton pump inhibitors, and TPN are also common modalities used (3,4). Several
studies report a high mortality rate in patients with black esophagus however death is rarely associated
with esophageal necrosis itself but rather from other underlying illnesses (1, 4, 7).
[Date]
The etiology of esophageal necrosis in our patient was likely secondary to ischemia due to cardiac
arrest. Treatment of the underlying problem resolves the disorder, therefore once hemodynamic
stability was maintained our patient improved and repeat endoscopy showed spontaneous resolution of
disease.
144
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Anushka Baruah, MD
An Unusual Case of Liver Abscess:
Anushka Baruah MD, Nyal Siddiqui DO
Case Report: A 37 year old African American gentleman with past medical history of recently diagnosed
right hepatic lobe abscess status-post pigtail catheter drainage and antibiotic therapy at an outside
hospital, presented with complaint of right upper quadrant abdominal pain and pus drainage at catheter
site. A CT scan of the abdomen demonstrated presence of a large multiloculated hepatic abscess
measuring 6.7 X 5.2 cms and an overlying right oblique intra-muscular abscess measuring 1.3 X 4.0 cms.
He denied fevers, chills, vomiting ,yellowish discoloration of skin, rash and weight loss. Laboratory tests
were consistent with anemia of chronic disease, low total proteins and albumin levels but negative for
abnormal liver enzymes and leucocytosis. He underwent abscess drainage with pigtail catheter
placement .Pus was sent for bacterial, fungal, acid fast bacilli , gram stain, PPD, echinococcus, entameba
serology and blood cultures were drawn as well. Meanwhile, we treated him with levofloxacin,
ceftriaxone and metronidazole. A CT scan repeated a week after initiation of antibiotics, revealed
worsening of the existing hepatic abscess, new smaller abscesses in the left lobe, and formation of
pulmonary nodules. During this time, fungal cultures started growing broad based budding yeast. A
diagnosis of blastomycosis liver abscess was made and the patient was put on amphotericin and
levofloxacin, followed by step-down therapy with itraconazole.
[Date]
Discussion: Blastomycosis is a systemic pyogranulomatous fungal infection, which is endemic to regions
around the Great Lakes, Lawrence, Mississippi and Ohio river basins. Historically, it was known as
Gilchrist’s disease, named after the man from Baltimore who discovered the fungus in 1894. This
condition more commonly affects males than females and children due to the nature of physical activity
they are involved in. Infection spreads through inhalation of infectious aerosolized conidia present in
wet soil or organic matter.While the most common locations of infection in descending order include
lung, skin and bone, blastomycosis is known to involve the reticuloendothelial system manifesting as
liver abscesses and splenic lesions in rare instances.Involvement of tissue other than lungs constitutes
disseminated disease. Histologically, the primary immune response to infection is seen as a mixed
inflammatory picture with polymorphonuclear cell predominance and resultant granuloma and
microabscess formation. Immunocompromised patients may not mount such an inflammatory response
to infection, so granulomatous lesions will characteristically be absent.Diagnosis is based on fungal
cultures and chemiluminescent DNA probe test. While azoles form the first line of therapy in most cases,
presence of immunocompromise, resistant infections and widespread dissemination warrant the use of
stronger antifungals like amphotericin B.It is pertinent to treat all patients with blastomycosis given the
long term implications of inadequate or lack of appropriate and timely management.
145
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Christopher W Bogan, MD
Neurosyphilis presenting as bipolar disorder in a young woman
First Author: Christopher W Bogan, MD Second Author: Alexandra Van Meter, MD
Introduction: Here we describe a case of neurosyphilis presenting as bipolar disorder, which is rare in
the antibiotic era.
Case description: A 36 year old female with no psychiatric or medical history presented to another
hospital with a 10 day history of erratic behavior, paranoid and erotomanic delusions, and hazardous
driving resulting in 2 motor vehicle accidents. She denied history of HIV, syphilis, or other sexually
transmitted diseases. She had no history of receiving treatment for syphilis. Initial evaluation
demonstrated an extremely labile and elated mood with pressured speech, delusional thought pattern,
and poor insight with impaired judgment. Medical workup was negative for organic etiology. Brain MRI
and EEG were both negative for acute processes. She was diagnosed with bipolar disorder and started
on lithium and olanzapine. Despite treatment, she continued to have mood lability and delusional
thinking. Her course was complicated by fever, tachycardia, physical exam findings consistent with
meningitis, and peripheral leukocytosis. A lumbar puncture (LP) was performed and showed WBC 23,
97% lymphocytes, glucose 90, and protein 44. She was transferred to our hospital for further
management.
On presentation, Acyclovir was started for possible viral meningitis, but CSF gram stain, HSV, and NMDA
antibody were negative and it was discontinued. With LP demonstrating a lymphocytic pleocytosis,
there was concern for neurosyphilis. Testing demonstrated a positive RPR at 1:128 and a positive serum
FTA-ABS. CSF VDRL was negative. She received 2 weeks of IV penicillin for neurosyphilis, and all
psychiatric medications were discontinued. At follow up visits, she was noted to have significantly
improved cognitive abilities and emotional functioning while being off psychiatric medications. Most
recently, she had an RPR titer of 1:32, indicating successful treatment of her disease.
Discussion: This case illustrates an unusual presentation of neurosyphilis as a psychiatric
disorder. Although the CSF-VDRL was negative in this case, neurosyphilis was considered to be the most
likely diagnosis based on the high RPR titer, positive FTA-ABS, and dramatic response to
treatment. Furthermore, CSF-VDRL may be falsely negative in up to 70% of patients with neurosyphilis.
Neurosyphilis and its psychiatric complications are rarely encountered in the present day. Since the
antibiotic era, the presentation is variable and includes neuropsychiatric symptoms, stroke, ophthalmic
symptoms, seizures, and spinal cord disease. In 1992, Roberts and Emsley presented 21 cases of
neurosyphilis, with personality changes and memory impairment being the most common presenting
symptoms. Saik et al. suggested that routine screening for syphilis should be considered for all
psychiatric patients.
[Date]
This case further exemplifies the importance of considering neurosyphilis in patients presenting with
psychiatric disorders.
146
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Camilo Cano Portillo, MD
To Drop or Not to Drop: Managing Severe Hypernatremia in the Setting of
Hyperosmolar Hyperglycemic State.
First Author: Camilo Cano Portillo, MD Venkat Rajasurya, MD Deepthi Gudivada
Hyperosmolar hyperglycemic state (HHS) is a life-threatening emergency manifested by marked
elevation of blood glucose, hyperosmolarity, and little or no ketosis. HHS is frequently associated with
hyponatremia. Management of severe hypernatremia in the setting of HHS can be challenging. There is
evidence that rapid normalization of serum sodium concentration can lead to cerebral edema. We
would like to present a case of a patient with HHS who also had severe hypernatremia. In such
situations, stepping outside established protocols may be necessary to achieve the desired outcome.
A 49 year old previously healthy woman came to the emergency department presenting with one week
of fatigue, dysuria, polyuria and diarrhea. On examination she appeared dehydrated and
disoriented. Her laboratory results were significant for 18000 white blood cells per mm3, serum glucose
of 800 mg/dl, corrected serum sodium of 177 meq/l, and serum osmolality of 405 mOsm/Kg. CT
abdomen revealed pyelonephritis, emphysematous cystitis, and mild sigmoid colitis. The patient was
admitted to the ICU and started on an insulin drip at 4 units/hour and on antibiotics. Her calculated free
water deficit was 8 liters. Our goal was to slowly modify the serum osmolality by careful correction of
the serum glucose and sodium. We did not want the rate of correction of the serum sodium to surpass
0.5 meq per hour. However, after initial resuscitation with half normal saline, we were unable to reach
the target rate of correction due to the patient's diarrhea. In consequence, we gave free water through
a nasogastric tube and unconventionally changed her intravenous fluids to dextrose 5%. This allowed us
to keep up with her free water losses. Once we had achieved the target sodium correction rate, we
started dextrose 5% with half normal saline and continued correcting her metabolic status. By day 3, the
patient’s serum osmolality had gradually reduced to 330 mOsm/L at the cost of maintaining her serum
glucose between 250 and 300 mg/dL and slowly reducing the serum sodium to 150 meq/L. Her mental
status became normal and there were no complications associated with our fluid management.
[Date]
Rapid correction of the serum sodium or serum osmolality in HHS can lead to cerebral edema due to
fluid shifts. Fluid and electrolyte management in HHS can be further complicated by additional
comorbidities. It is necessary to alter the usual composition and administration rates of fluids depending
on the feedback obtained from frequent monitoring of the serum osmolality and corrected
sodium. Slow correction of the metabolic abnormalities is necessary to prevent adverse consequences.
147
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Samaneh Dowlatshahi, MD
Thyroid Hormone Resistance: A Case Report
Samaneh Dowlatshahi, MD, SeyedAmirHossein AfsharImani, MD
Objective: Resistance to thyroid hormone is a rare condition caused by tissue refractoriness to the
effects of circulating thyroid hormone, and may be misdiagnosed as hyperthyroidism. This syndrome is
characterized by elevated circulating thyroid hormones, and unsuppressed TSH levels. Although most
patients are euthyroid, rarely they may present with clinical hyperthyroidism, if the pituitary gland is
more insensitive than other tissues to thyroid hormones. In this study we present a case of thyroid
hormone resistance with clinical evidence of hyperthyroidism.
Methods: We present a case of 58 year old male who suffered from thyrotoxicosis for many years.
Case Presentation: A 58 year old male who suffered from thyrotoxicosis and diarrhea for many years
and had been under treatment for atrial fibrillation with rate control medications. He had been tested
for thyroid function in the past which revealed elevated fT3 and fT4 with slightly elevated TSH
concentration. Pituitary adenoma was excluded as magnetic resonance imaging showed normal
pituitary gland, alpha subunit was within normal range and TSH concentration increased after TRH
administration. Sonography revealed normoechogenic, slightly enlarged thyroid gland. Methimazole had
been tried in the past without any significant improvement. The diagnosis of thyroid hormone resistance
was made and he was started on bromocriptine at a dose of 10 mg per day. After 2 months of treatment
he achieved a state of constant euthyrosis and following next few months thyroid volume diminished.
Discussion: Failure to differentiate thyroid hormone resistance from primary thyrotoxicosis has resulted
in the inappropriate treatment of nearly one-third of patients. Also, the diagnosis allows appropriate
genetic counselling, and initiation of treatment.
[Date]
Conclusion: In this case report we emphasize the importance of timely diagnosis of thyroid hormone
resistance, which prevents many patients from being wrongly diagnosed as Graves disease and
therefore various inappropriate treatments. Also, we present a successful treatment of this rare
condition with bromocripten
148
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Samaneh Dowlatshahi, MD
Successful Treatment of an Acute Hypertriglyceridemia-Induced Pancreatitis Using
Insulin and Heparin Infusion
First Author: Samaneh Dowlatshahi, MD
Objective: Hypertriglyceridemia over 1,000 mg/dl can provoke acute pancreatitis and its persistence can
worsen the clinical outcome. There are no clinical guidelines to severe hypertrigliceridemia, but therapy
with insulin, heparin, a combination of both, plasmapheresis, or octreotide have been tested
succesfully.
Methods: We report a case of a 43-year-old female with clinical acute pancreatitis along with incidental
finding of an severe hypertrigliceridemia , who had a good outcome after treatment with insulin, and
heparin intravenous infusion.
Case Presentation: A 43-year-old female with previous history of acute pancreatitis, was admitted to
Intensive Care Unit (ICU) because of severe abdominal pain, anorexia, vomiting, and hyperventilation.
She was diagnosed with acute pancreatitis. Her laboratory tests revealed: Amylase: 1740 (25-125 IU/L),
Lipase: 536 (0.0-6 IU/L), Anion Gap: 10 (10-20 mmol/l), Glucose: 110 mg/dl, normal liver function panel,
HbA1c: 5.2% (<5.7). Ultrasound showed evidence of pancrease edema consistent with acute
pancreatitis, there was no evidence of cholelithiasis, common bile duct dilatation, or cholecystitis.
Patient was diagnosed with acute pancreatitis. Treatment was initiated with fasting, gastric
decompression by nasogastric tube, normal saline infusion with rate of 125 cc/h, and analgesia with
morphine. Her fasting lipid profile the next day revealed: Triglyceride: 18000 mg/dl, and total
cholesterol: 970 mg/dl. Patient was started on insulin and heparin drip, and dextrose 5% infusion.
Triglyceride levels decreased progressively so insulin infusion remained at 0.5 to 1iu/kg/h. At 48 hours,
TGC levels dropped to 6174,and decreased to 476 at 96 hours during her stay in ICU, there were no
neurological disorders, respiratory or kidney problems, and she did not experience abdominal pain after
discontinuation of analgesia within 24 hours after admission. There were no bleeding and no clinical or
laboratory signs of infection.. She was discharged from the ICU after 72 hours, following clinical
stabilization, and remained stable on floor where she remained hospitalized for 1 week. She was
discharged with prescription of gemfibrozil 600 mg twice daily.
[Date]
Discussion: In this case report, the triglyceride levels of 18000 was succefully treated with combination
of insulin and heparin drip. Both activate the lipoprotein lipase enzyme (LPL) bound to endothelium. In
addition, heparin mobilizes and releases the enzyme of the endothelium to plasma. Insulin promotes the
synthesis of LPL and stimulates the uptake of fatty acids released from triglyceride hydrolysis by LPL
itself
149
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Amrutha Mary George, MD
Colistin Induced Hypercapnic Respiratory Failure: Old Drug, Toxicity Revisited
Amrutha Mary George Jacob, Patricia Macias, Amith George Jacob
INTRODUCTION: Increase in multidrug resistant gram negative bacilli has led to the re-emergence of
colistin use in sepsis. Colistin neurotoxicity can prolong ventilator dependance by causing respiratory
failure. We report a novel case of colistin toxicity presenting as hypercapnic respiratory failure
CASE PRESENTATION: A 75 year old on dialysis presented with abdominal pain and intermittent fevers
for 3 days. On examination she was febrile, tachycardic, tachypneic and hypotensive with right upper
quadrant abdominal tenderness. Laboratory investigations revealed leukocytosis with bandemia. She
was started on crystalloids, pressors, vancomycin, piperacillin-tazobactam. Further workup revealed
cholangitis for which she underwent endoscopic drainage. On day 2 of admission blood cultures were
positive for Klebsiella Pneumoniae resistant to carbapenemase for which colistin therapy was started
On day 4 she developed sudden hypercapnic respiratory failure requiring intubation. A-a gradient was
normal on ABG raising concern for neuromuscular disorder or hypoventilation. No obvious cause for
respiratory deterioration was identified. A diaphragmatic EMG revealed low action potential with
normal conduction velocities. Given duration and timing of clinical deterioration critical care myopathy
was unlikely. Colistin induced neurotoxicity was suspected and she was switched to gentamicin. She
improved in 48 hours and was successfully extubated. Rest of her hospitalization was uneventful
DISCUSSION: Respiratory failure from colistin associated toxicity is seldom reported. Neurotoxicity
incidence from the largest study till date is 7.3%1. Colistin acts via disruption of cholesterol cell
membranes making highly lipid rich neurons more vulnerable to toxicity. Proposed mechanism of
colistin neurotoxicity involves blockade of presynaptic acetylcholine release, usually exacerbated by
renal disease, hypocalcemia or use of other neurotoxic drugs. Respiratory muscle paralysis is more
common when administered to critically ill patients with multiple comorbidities and can occur with both
parenteral or inhaled2 forms. Cases usually present with respiratory muscle fatigue that progresses to
apnea and is more common in patients with renal disease3 given the fact that colistin is renally cleared
CONCLUSIONS: In our patient the time-frame of events and recovery following discontinuation of
colistin were not suggestive of critical care myopathy. Though most common side effects are nausea and
nephrotoxicity physicians need to be aware of possible neurotoxicity especially given its frequent use in
the multi-drug resistant microbial era


Reference #1 : Falagas et al.Toxicity of polymyxins:a systematic review of the evidence from old and recent studies.Crit Care 2006

Reference #3: Lindesmith et al.Reversible respiratory paralysis associated with polymyxin therapy.Ann Int Med 1968
[Date]
Reference #2: Koch-Weser et al.Adverse effects of sodium colistimethate:manifestations and specific reaction rates during 317
courses of therapy.Ann Intern Med 1970
150
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Baqer Haider, MBBS
An outlier of inflammatory arthropathy in Coxsackie B infection.
First Author: Baqer Haider, Second Author: Aaron Maki
Introduction: Coxsackie B infections have been known to present with varied clinical manifestations
including myopericarditis, meningoencephalitis and polymyositis, however arthropathy has not been
widely recognized with only 11 cases reported.
Case: An 18-year-old African American male presented to the hospital with complaints of fever,
vomiting, weakness in his upper and lower extremities, unsteady gait and joint pain. A few days prior to
the onset of symptoms he had a diarrheal illness. He denies any recent history of travel, sick contacts,
animal bites, scratches or insect bites. Physical examination revealed scattered non-confluent macules
less than 1cm on upper chest and arms bilaterally. Bilateral tenderness and swelling was present in
shoulder, knee and ankle joints. Motor strength was noted to be 2/5 in the upper and lower extremities.
Investigations revealed pancytopenia, creatinine kinase of 22,000 U/L, transaminitis and impaired renal
function secondary to rhabdomyolysis. Myositis specific antibodies were negative along with connective
tissue disease panel. Bacteriological studies yielded negative results and viral studies showed, apart
from a past parvovirus B19 infection, positive Coxsackie B4 titers at 1:16 and B6 titers at 1:8. Initially
there was suspicion of hemophagocytic syndrome and possibly dermatomyositis; however, patient’s
rash was not typical and scant factors in support. An echocardiogram demonstrated a low normal
ejection fraction of 45-50% with mild global hypokinesis. He was given aggressive intravenous hydration
which resulted in shortness of breath; with diuresis his respiratory symptoms improved. Intravenous
infusion of methylprednisolone 125mg every eight hours was begun and within a 24 hour period his
muscle enzymes trended downwards and his inflammatory myopathy and arthropathy gradually
improved. He was discharged 3 days later in stable condition on oral prednisone 80mg daily. He was
seen one week later as an outpatient with complete resolution of symptoms and prednisone was
tapered. Four weeks later Coxsackie B titers were rechecked and found to be negative at B4 < 1:8 and B6
<1:8.
[Date]
Discussion: This case represents features strikingly outside the realm of a usual Coxsackie B infection
and therefore of great importance to a wide range of physicians. Coxsackie B viruses are both highly
resistant to chemical treatment and highly contagious primarily through the fecal-oral route, so a high
index of suspicion for unusual presentations of this infection may aid in the timely diagnosis and
treatment of this potentially fatal disease.
151
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Abdalla Hassan, MD
Rapidly Progressive Multicenteric Castleman’s Disease in Patient with Acute
Retroviral Syndrome: A Case Report
Carroll Christie, MD Abdalla Hassan, MD
Introduction: Multicenteric Castleman’s Disease (MCD) is a lymphoproliferative disorder that occurs
more frequently in Human Herpes Virus-8 (HHV-8) positive HIV patients. We are reporting a unique case
of rapidly progressive Multicenteric Castleman’s disease in a patient with acute retroviral syndrome
(AVR).
Case Presentation: A 40-year-old homosexual male presented to our institution with fevers, chills and a
syncopal episode. The patient had a history of hypertension, illicit drug use, and was recently diagnosed
as having HIV. Two weeks prior to his admission, he experienced an episode of syncope, followed by 5
days of fever and chills and diffuse body aches. He also reported having a negative HIV test 2 months
earlier. On presentation, he was febrile and tachycardic. Physical examination demonstrated right-sided
non-tender cervical lymphadenopathy with hepatosplenomegaly. His labs were significant for
pancytopenia (WBC of 4.1 thousand/mcL; HgB 6.1 gm/dL; Platelet 78 thousand/mcL), hyponatremia
(131 mmol/L), and creatinine of 1.5 mg/dL. At that time, the working diagnosis was Anti Retroviral
Syndrome (AVR) , however, transfusion refractory anemia is not a characteristic of AVR . Peripheral
blood smear showed spherocytosis, and iron studies were significant for anemia of chronic
disease. Moreover, computed tomography showed hepatosplenomegaly with multiple enlarged lymph
nodes in the abdomen and pelvis. Lymph node biopsy was obtained and was consistent with HHV-8associated Multicentric Castleman’s disease. The patient started anti-retroviral therapy for HIV, and
Gancyclovir and Rituxamab for MCD. Two days later, he continued to deteriorate and had drops in
hemoglobin and platelets requiring multiple transfusions. The patient developed severe respiratory
distress requiring intubation and transfer to an intensive care unit; however, after four days, the patient
expired.
[Date]
Discussion: Castleman's disease is also known as angiofollicular hyperplasia, and is non-clonal disease of
the lymph nodes. The exact pathophysiology of MCD is still controversial, with IL-6 hypersecretion
playing a major role. The association between chronic HIV and HHV-8-associated Castleman’s disease is
well documented in the literature; however, no prior cases reported rapidly progressive Multicenteric
Castleman’s disease in AVR. This case provides evidence of the occurrence of MCD in AVR and its
associated poor prognosis.
152
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Abdalla Hassan, MD
Two Lumens-One Artery, Spontaneous Spiral Coronary Artery Dissection in MiddleAge Female Presenting with Unstable Angina: Case Report
Abdalla Hassan, MD Ahmad Parvinian, MD
Introduction: Spontaneous coronary artery dissection (SCAD) is an uncommon and challenging clinical
entity. It has a striking predilection for young, otherwise healthy female patients with a mean age of 3540 years. Herein, we present a case of acute coronary syndrome secondary to SCAD.
Case presentation: A 51-year-old female with a history of hyperlipidemia presented to our emergency
department with chest pain that began several hours previously while she was seated at her desk. She
described the pain as a retrosternal "burning" sensation with radiation to the left shoulder and neck. It
was associated with nausea and lasted approximately 20 minutes before subsiding spontaneously.
Physical examination was unremarkable. Her vitals were normal. The initial EKG revealed normal sinus
rhythm without ischemic changes. The troponin level was 0.18 ng/mL. Two hours later, the patient's
chest pain recurred, with her heart rate and blood pressure rising to 97 BPM and 143/71 mm Hg,
respectively. Repeat EKG showed new T-wave inversions in the anteroseptal leads and the troponin level
rose to 1.02 ng/mL, peaking three hours later at 1.28 ng/mL. Her echocardiogram was normal. The
patient was treated with aspirin, a beta-blocker, and a statin, and was started on heparin and
nitroglycerin drips. The following day she underwent coronary angiography, which revealed spiral
dissection of the mid- to distal LAD and proximal RCA vasospasm that resolved with intracoronary
nitroglycerin infusion. Afterwards, she remained asymptomatic and was treated conservatively with a
regimen consisting of aspirin, clopidogrel, a beta-blocker, a statin, and isosorbide mononitrate, as well
as amlodipine for coronary spasm.
[Date]
Discussion: The overall incidence of SCAD in angiographic series ranges from 0.28 % to 1.1 %. The clinical
presentation of SCAD is variable and ranges from unstable angina to sudden cardiac death. The most
common conditions associated with SCAD are coronary atherosclerosis and the peripartum period. The
theory underlying the association between atherosclerosis and coronary artery dissection is that
atherosclerotic plaque inflammation and rupture may disrupt the intimal-medial junction, resulting in
intimal flap formation and intramural hematoma. The prognosis of patients with SCAD has improved in
recent years, with a recent analysis demonstrating a survival rate approaching 90%. The choice of
treatment must be individualized based on both clinical and angiographic factors. In conclusion, SCAD is
a rare yet important cause of unstable angina, myocardial infarction, and even sudden death. It is
paramount that physicians maintain an awareness of this entity when presented with patients
complaining of chest pain and who lack classical risk factors.
153
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Laura N Hernandez, MD
A case of Strongyloides Hyperinfection leading to diffuse alveolar hemorrhage and
appendicitis.
First Author: Laura N Hernandez, MD Neha Jaswal, MD
Strongyloides is a neglected tropical disease often overlooked in the developed world. In
immunocompromised patients, it can present as hyperinfection syndrome, meaning Strongyloides
larvae are confined to organs normally involved in the pulmonary autoinfection cycle (i.e., GI tract,
lungs, and peritoneum). Mortality from hyperinfection is as high as 87%. Prompt recognition and
treatment are important to decrease mortality. Steroid use is associated with hyperinfection. While HIV
infection is associated with Strongyloides infection, it does not appear to increase risk of hyperinfection.
We report a case of young man with AIDS presenting with dyspnea and melena, found to have
hyperinfection syndrome with development of diffuse alveolar hemorrhage, ARDS and appendicitis.
33-year-old man of Mexican origin with history of advanced AIDS diagnosed in 2012, high viral load, and
CNS toxoplasmosis who was receiving corticosteroids presented with complaints of shortness of breath,
fever, diarrhea and melena for one week. He was septic and hypoxic. Stool guaiac was positive. Routine
lab were notable due to a 6 gram drop in hemoglobin over two weeks, mild leukopenia and moderate
hyponatremia. Chest x-ray revealed diffuse patchy infiltrates. He required intubation for respiratory
failure and vasopressors. He underwent diagnostic bronchoscopy and bronchoalveolar lavage revealing
bloody lavage. Esophagogastroduodenoscopy showed friable mucosa with ulcerations. Blood culture
grew Pseudomonas aeruginosa. Stool for ova and parasites came back positive for Strongyloides
stercolaris. The parasite was also seen in BAL samples and duodenal pathology. He was Initially covered
with broad-spectrum antibiotic then narrowed down based on the sensitivity pattern. Ivermectin was
started for Strongyloides treatment. Hospital course was complicated by right lower quadrant pain. CT
scan of the abdomen showed free air in the peritoneal cavity. He was taken for emergent exploratory
laparotomy showing perforated appendix and pathology revealed the parasite. He was treated with
ivermectin for two weeks including rectal enema with clearance of the parasite and successfully
discharged.
[Date]
Various cases of strongyloides hyperinfection have been described in the literature presenting as diffuse
alveolar hemorrhage, ARDS, abdominal pain, gastrointestinal bleeding and perforation. Gram Negative
sepsis is also part of the spectrum due to either disruption of the bowel wall, allowing entrance of the
bacteria to the systemic circulation, or adherence of the bacteria to the larvae surface during parasite
migration. Appendicitis is a very uncommon presentation of hyperinfection syndrome. On literature
search we found two case series describing the various organ involvement but none described diffuse
alveolar hemorrhage and appendicitis as initial presentation. Our case is also unique in terms that rectal
ivermectin enema was used when patient developed paralytic ileus. Only few cases have been described
to use rectal formulation of ivermectin. This case illustrates the importance of considering uncommon
pathogens in immunosuppressed patients presenting with multisystem involvement.
154
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Janet Jang, MD
Connecting the dots - a case of autoimmune polyglandular syndrome type II
First Author: Janet Jang, MD Second Author: Dhananjay, Kulkarni, MD
Introduction: Autoimmune Polyglandular Syndrome (APS) Type II is characterized by Addison’s disease
with autoimmune thyroid diseases and/or type I Diabetes Mellitus. It is a rare disease with prevalence of
14-20 cases per million in the United States. In APS type II, about 56% of patients present with Addison’s
disease with chronic thyroiditis and about 11% present with the complete triad.
Case description: A 33 year old female with no significant past medical history presented to her primary
care physician’s office with chief complaint of nausea, vomiting, and weight loss over the past two
months. She was feeling fatigued and light-headed. On physical examination, she was hypotensive with
a blood pressure of 80/54. She was not in acute distress and there was no thyroid enlargement or
nodularity. Heart rate and rhythm were regular with no murmurs. Neurological exam revealed no focal
findings. Labs revealed a TSH >100, free T4 of 0.4, and sodium level of 121. She was admitted for further
evaluation. She was started on intravenous fluids but remained hypotensive. Laboratory tests revealed
low random cortisol level of 2.58, hyponatremia and high normal potassium levels. Endocrinology was
consulted and she was started on IV dexamethasone for adrenal insufficiency. She responded well and
was continued with tapering dose of hydrocortisone. During the course of hospitalization, anti-thyroidperoxidase antibody was positive suggesting autoimmune thyroiditis. She was started on levothyroxine
for primary hypothyroidism. Upon subsequent evaluation, anti-21 hydroxylase antibody was positive,
supporting diagnosis of autoimmune Addison’s disease.
Discussion: APS type II is a familial condition in nature and is often transmitted as an autosomal
dominant trait with incomplete penetrance. It usually occurs in the third to fourth decade of life and has
a female predominance with female: male ratio of 2.7-3.7:1. HLA-DR3 and HLA-DR4 increase disease
susceptibility. Laboratory investigations include electrolytes, anti-thyroid peroxidase, anti-21
hydroxylase, and anti-glutamic acid decarboxylase antibodies. Imaging studies such as CT scan can be
utilized to look for abnormalities of adrenal gland. Treatment involves hormone replacement therapy in
most cases.
[Date]
Patients with a new diagnosis of hypothyroidism should be evaluated for adrenal insufficiency if there
are suggestive clinical symptoms such as weight loss (which is not typical of hypothyroidism), persistent
hypotension despite fluid resuscitation, along with high or high normal potassium levels accompanying
hyponatremia, such as in our case. This is crucial because if Addison’s disease and hypothyroidism do
occur concurrently, administration of thyroid hormone without replacing glucocorticoids, can
precipitate adrenal crisis by the action of thyroxine in enhancing hepatic corticosteroid metabolism.
Therefore it is crucial that such patients be treated with glucocorticoids prior to thyroid hormone
therapy. If these conditions are identified together, further work up for APS is warranted.
155
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Sima Kavand, MD
Double trouble: A case of DRESS syndrome with overlapping Steven Johnson’s
syndrome
First Author: Sima Kavand, MD Second Author: Charles Vainder, MD
Drug reaction with eosinophilia and systemic symptoms (DRESS) and Steven Johnson’s Syndrome (SJS)
are two distinct cutaneous drug reactions. In this abstract, we report a patient with hypersensitivity
reaction to phenytoin with clinical findings of both syndromes.
A 36 year old male with diabetes mellitus and recently onset seizure was admitted to our hospital with
fever, diarrhea and maculopapular rash, started two days prior to arrival. Drug history was remarkable
for phenytoin, started recently for seizure disorder and insulin. In examination, patient appeared ill with
facial edema. There was generalized morbilliform eruption over the trunk and extremities. In blood test,
He had elevated WBC with eosinophilia, elevated liver enzymes, serum creatinine and CRP. One day
after admission, he developed erosive lesions over his lips and buccal mucosa and epidermal loss of his
scrotal skin. Biopsy of skin lesion was consistent with SJS. Diagnosis of DRESS syndrome was proposed
based on the clinical and laboratory features and recent exposure to phenytoin, although the mucosal
involvement and epidermal loss was also suggested an overlapping feature with SJS. Phenytoin was
replaced by Keppra and Prednisone 40 mg daily was started for the patient. One week later, the patient
was discharged from the hospital with tapering dose of Prednisone while he was clinically improving.
[Date]
This case demonstrates the fact that adverse cutaneous drug reaction can sometimes present with an
overlapping feature. Although determining the causative agent is more critical than a precise diagnosis,
having specific diagnosis for every clinical encounter is very essential.
156
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Sathish Kumar Krishnan, MD
It Is Not The Plasmodium That Dropped The Counts – A Case Of Hemophagocytic
Syndrome.
First Author: Sathish Kumar Krishnan, MD Second Author: Dhileepan Selvarajan, MD Third Author:
Praveen Jayapal, MBBS
Introduction: Hemophagocytic lymphohistiocytosis (HLH) is a hyperinflammatory syndrome caused by
excessive cytokine production due to highly activated but ineffective immune process. It is an aggressive
and life threatening condition. High index of suspicion is needed to diagnose the condition which is
potentially treatable.
Case description: A 24-year-old male presented to the Emergency Department with a 5-day-history of
intermittent fever and abdominal pain. The history was significant for recent travel to India. His vitals
were BP: 106/84 mmHg, HR: 106/min, RR: 18/min and temp: 101.2 F. His physical examination was
significant for pallor, left upper quadrant tenderness and moderate splenomegaly. Complete Blood
Count revealed pancytopenia – Hb: 9.0 g/dL, WBC: 3000/dL and platelets: 80000/dL. Liver function test
was remarkable for direct hyperbilirubinemia and mild transaminitis. Peripheral smear examination
showed plasmodium falciparum. He was treated with artesunate. He was hemodynamically stable and
his fever resolved, but his pancytopenia worsened. On day 4, his complete blood count was Hb: 7.2 g/dL,
WBC 2600/dL and platelet 36000/dL. He developed confusion, petechiae, ecchymoses and spontaneous
gum bleeding. In view of worsening pancytopenia, a bone marrow biopsy was performed, which
revealed numerous hemophagocytes with the malarial gametocytes. His ferritin and triglyceride level
were also found to be significantly elevated. A diagnosis of HLH was made and was treated with high
dose dexamethasone. He clinically improved and the pancytopenia resolved.
[Date]
Discussion: Hemophagocytic lymphohistiocytosis can be of two types – familial and secondary. Familial
occurs mostly in children less than 5 years of age. Secondary HLH occurs mostly in adults due to
bacterial, viral and parasitic infections, and malignancies. The diagnosis needs five of the following
features – fever, splenomegaly, pancytopenia, hypertriglyceridemia/hypofibrinigonemia, elevated
ferritin, elevated CD 25, absent natural killer (NK) cell activity and hemophagocytes in the bone marrow
exam. Patients can also have altered mental status, seizure, lymphadenopathy, skin rashes, jaundice,
acute kidney injury, multi-organ dysfunction and ARDS. Secondary HLH can be easily missed as many
infections can cause cytopenia and many features of the disease can occur in sepsis. So, persistent
cytopenia and lack of improvement with appropriate therapy should heighten the suspicion for HLH.
Prompt recognition and treatment with high dose dexamethasone has shown to improve outcome.
157
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Aman Kugasia, MD
Systemic lupus erythematosus, psoriasis, psoriatic arthritis successfully treated
with Ustekinumab.
First Author: Aman Kugasia, MD, Udit Yadav, MD, Meenakshi Jolly, MD.
FDA has approved ustekinumab for the treatment of moderate to severe plaque psoriasis. It is a human
monoclonal antibody that inhibits interleukins 12 and 23, which are involved in the TH-17 signaling
pathway. There have been case reports of subcutaneous lupus erythematosus(SCLE) successfully treated
with ustekinumab indicating involvement of TH-17 pathway in the pathogenesis of SCLE. Here we report
the first known case of successful treatment of psoriasis, psoriatic arthritis and systemic lupus
erythematosus (SLE) with ustekinumab.
A 48 year old gentleman with psoriasis and psoriatic arthritis involving both knees and arthralgia of small
joints of hands came to the rheumatology clinic for the management of arthritis. Patient’s past medical
history was significant for autoimmune hemolytic anemia treated with rituximab 7 years ago,
thrombocytopenia and recurrent inflammatory knee effusions. Physical exam was significant for
erythematous scaly plaques covering both elbows and lower back and moderate left knee effusion. Labs
were remarkable for thrombocytopenia (52000 cells/microliter), positive anti-nuclear antibody (1:640)
and anti ds-DNA antibody. Patient had not responded to etanercept for psoriatic skin lesions in the past
and at that point he was taking infliximab. Diagnosis of SLE was made based on hemolytic anemia,
thrombocytopenia, positive antinuclear antibody,positive anti ds-DNA antibody and arthralgia.
Treatment with infliximab was stopped due to concern for drug induced lupus. Patient was started on
mycophenolate mofetil and prednisone for treatment of SLE. Meanwhile, cyclosporin was started by
dermatology for the management of psoriatic skin lesions so mycophenolate mofetil was discontinued
to avoid excessive immunosuppression. Patient was showing modest improvement in the skin and joint
lesions along with improvement in platelet counts. After three months, we initiated ustekinumab as a
steroid sparing agent to treat lupus along with psoriasis and psoriatic arthritis so cyclosporin was
discontinued and prednisone was tapered off. After three doses of ustekinumab there was complete
resolution of skin lesions and normalization of platelet count. However due to persistent left knee
arthritis, methotrexate was added to ustekinumab. After two months of treatment with ustekinumab
and methotrexate patient knee arthritis has also resolved. Patient has been on current regimen for the
past 30 months without any recurrence of psoriatic lesions, thrombocytopenia or hemolytic anemia. No
medication related adverse effect were noted during this period.
[Date]
Recently a subset of T cells, distinct from T helper (TH)1 and TH2 cells, producing interleukin (IL)-17 (TH17)
was defined and seems to have a crucial role in mediating autoimmunity and inducing tissue
inflammation. Ustekinumab acts by inhibiting interleukins 12 and 23, ultimately leading to TH-17
pathway blockage. Manifestation of SLE has responded well to ustekinumab highlighting fact that there
may be role of TH-17 blocking agents in the management of SLE. Further research is needed to
characterize specific subset of SLE patients who may benefit from TH-17 pathway blockage.
158
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Mohamad Hani Lababidi, MD
A severe case of Microscopic Polyangitis causing diffuse alveolar hemorrhage and
anemia
First Author: Mohamad Hani Lababidi, MD, Chukwuka Okolo, MD
Learning objective: - Diffuse alveolar hemorrhage should be considered in pts who develop progressive dyspnea
with alveolar opacities on chest imaging. - Pulmonary and renal involvement suggests a multisystem disease. Small-vessel vasculitis should be suspected in any patient who presents with a multisystem disease that is not
caused by an infectious or malignant process Introduction: - ANCA-associated vasculitides include granulomatosis
with polyangiitis (Wegener's or GPA), microscopic polyangiitis (MPA), Churg-Strauss syndrome (CSS) and renallimited vasculitis. - MPA is a systemic necrotizing vasculitis characterised by inflammation of the small blood
vessels, the absence of granulommas on histopathology, and the presence of circulating anti-neutrophil
cytoplasmic antibodies (ANCAs).
Case presentation: - A 58 year old male otherwise healthy presented to the ED with 5 day history of exertional
dyspnea and non-productive cough associated with fever and night sweats. He also reported 12 pounds weight
loss for the past 1 month. Does not use any medications. He is a previous smoker of 1 PPD for 20 years. - On
admission he was febrile, T 101.7, HR 106, RR 24, BP 156/80, O2 sat 97%. - PE was significant for tachypnea, pale
conjunctiva and dry mucous membranes. - In the ED he was found to have a Hgb of 5.4 elevated Cr of 7.2 and his
CXR showed bilateral pulmonary infiltrates. UA on admission also showed large proteinuria and large hematuria. Pt
was transfused with 2 units of PRBCs and was started on empiric Abx for possible pneumonia. Iron studies showed
anemia of chronic disease. - Further workup was as following: HIV (neg), Hepatitis panel (neg), TB Quantiferon
(neg), Anti-GBM Ab (neg), Anti-dsDNA Ab (neg), PR3-ANCA (neg), MPO-ANCA positive. Pt was admitted to the
medical floor, however, on the same day he desaturated down to 88% on 4L NC with tachypnea and confusion.
Stat CXR was obtained that showed greatly worsening infiltrates compared to admission. - Pt was transferred to
the ICU and intubated. Received high dose steroids (1 gm solumedrol daily x 3 days then prednisone 60 mg daily),
cyclophosphamide (75 mg BID) and started on plasmapheresis (x 7 days). Atovaquone for PCP ppx. He received
further PRBC transfusions for drop of his Hgb (5 Units total) and 20 units of FFP. Bronchoscopy revealed diffuse
blood oozing from all pulmonary segments, consistent with pulmonary hemorrhage. Kidney biopsy was performed
that showed Pauci-immune crecenteric GN (which is typical for MPA)
[Date]
Discussion: - Micriscopic Polyangitis is the most common cause of the pulmonary-renal syndrome of alveolar
hemorrhage and rapidly progressive glomerulonephritis. - Peak incidence age 30-50 years, Incidence 8 cases per
million - Triggered by Infections, Drug and toxins (propylthiouracil, hydralazine, cocaine, silica). - Targets of ANCA
are protienase 3 and myeloperoxidase in the neutrophils and monocytes granules causing there activation and
further damage of the vacular walls. - Manifests as: Glomerulonephritis (nearly 80% of patients), Weight loss
(>70%), Mononeuritis multiplex (60%), Fevers (55%),Cutaneous vasculitis (>60%), Alveolar hemorrhage, in
contrast,occurs in only about 12% of patients. - corticosteroids and immunosuppressants cyclophosphamide)are
the mainstay of therapy, plasma exchange, in severe DAH.
159
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE John J Lee, MD
Beware of Wild cARDS: Blastomycosis
First Author: John J Lee, MD Vaishnavy Bhaskaruni, Kaveh Tayebi, Sindhu Joseph. MacNeal Hospital,
Berwyn, IL.
Blastomycosis is a pyogranulomatous disease caused by Blastomyces dermatitidis. Its clinical
presentation ranges from asymptomatic to severe respiratory failure. This case reports Blastomycosis
related Acute Respiratory Distress Syndrome in a previously healthy patient.
A previously healthy 58 year old male presented with increasing dyspnea for three days. On admission,
his heart rate was 110, respiratory rate was 19, and his oxygen saturation was 85% on room air. Chest xray revealed bilateral coarse interstitial infiltrates. The patient was started on Vancomycin, Levofloxacin,
and Piperacillin-Tazobactam. During the hospital stay, the patient became increasingly hypoxic, with
rapid respiratory deterioration. Empiric intravenous steroids were initiated with no clinical
improvement. A computed tomography of the thorax was obtained, which revealed bilateral patchy
lung consolidation. Bronchoscopy was non-revealing, and the studies from bronchoalveolar lavage (BAL)
including fungal culture were negative. Given the lack of clinical improvement, an open lung biopsy was
done, with pathology revealing blastomycosis. Immediately after surgery, the patient developed severe
respiratory failure consistent with ARDS. Liposomal Amphotericin B treatment replaced antibiotics and
intravenous methylprednisolone was continued. The patient’s PaO2/FiO2 ratio gradually improved, and
he was successfully extubated one week later. Methylprednisone was tapered, and converted to oral
prednisone. The patient will be on liposomal amphotericin for 28 days and itraconazole for one year
thereafter.
Our case presented an unusual diagnostic challenge with Blastomycosis. In one case series, 100% of
cultures obtained from bronchoalveolar lavage yielded the organism in patients who were known to
have pulmonary blastomycosis. In our case, the bronchial washing fungal culture and smear were
negative. The diagnosis was only made after the lung biopsy. Moreover, blastomycosis infrequently
presents as Acute Respiratory Distress Syndrome, especially in immunocompetent patients. In previous
case reports, blastomycosis-related ARDS cases were associated with a mortality rate of 50-89%, when
antifungal therapy without adjunctive corticosteroids treatment regimen was employed. In contrast,
two case reports show better efficacy when corticotherapy is combined with antifungal therapy. It is
presumed that corticotherapy reduces inflammation, a core component of ARDS. In fungal infections,
inflammation is likely secondary to host cell mediated immunity, and it is proposed that steroids subdue
such a reaction and therefore, increase gas exchange.
[Date]
Blastomycosis can present in a myriad of forms and may pose a diagnostic challenge. Although
bronchoalveolar washings are associated with a high yield in identifying blastomycosis, if there is a high
clinical suspicion, a negative bronchoalveolar lavage should warrant immediate lung biopsy to avoid
delay in diagnosis and subsequent treatment. Blastomycosis infrequently present as ARDS and in such
cases, corticotherapy in adjunction to antifungal therapy should be strongly considered.
160
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Nanditha N Malakkla, MD
Esophageal Perforation as a Complication of Colonoscopy
First Author: Nanditha Malakkla, MD. Chandramohan Meenakshisundaram, MD
Learning Objectives: To identify that Boerhaave’s syndrome can be a rare complication of routine
colonoscopy, and to discuss the manifestations, diagnosis, and treatment of Boerhaave’s syndrome.
Case: 76 y o female with no significant past medical history underwent outpatient screening
colonoscopy. Procedure was difficult due to tortuous colon and only multiple diverticula were visualized.
She vomited once during the procedure and postoperatively she felt nauseous and had dry heaves.
Shortly after, she complained of neck swelling. Her vital signs were stable. On examination she had right
sided neck and facial swelling with palpable crepitations over neck and upper chest as well as coarse
breath sounds on auscultation of both lung fields. Cardiac and abdominal exam was unremarkable.
Emergent CT chest showed extensive subcutaneous air within the soft tissues of the neck bilaterally,
extending into the mediastinum and along the anterior chest wall. An esophagram revealed a focus of
oral contrast actively extravasating approximately at 2.5 cm above the gastroesophageal junction
consistent with a small perforation. She underwent left thoracotomy with esophageal repair. She was on
total parenteral nutrition (TPN) for a week which was later transitioned to pureed diet. Further hospital
course was uncomplicated and she was discharged to a subacute rehabilitation facility.
[Date]
Discussion: Boerhaave's syndrome is a spontaneous perforation of the esophagus due to sudden
increase in intraesophageal pressure combined with negative intrathoracic pressure caused by straining
or vomiting. The tear usually occurs at the left posterolateral wall of the lower third of the esophagus.
Usually patients have severe retching and vomiting which is followed by excruciating retrosternal chest
and upper abdominal pain after perforation. Other manifestations are odynophagia, tachypnea,
dyspnea, fever, and shock. On physical examination subcutaneous emphysema (crepitation) is an
important diagnostic feature. Chest radiograph usually reveals mediastinal or free peritoneal air as the
initial manifestation, and hours to days later pleural effusion with or without pneumothorax, widened
mediastinum, and subcutaneous emphysema are typically seen. The diagnosis of esophageal perforation
can also be confirmed by water-soluble contrast esophagram using Gastrografin, which reveals the
location and extent of extravasation of contrast. Treatment depends upon the size and location of the
perforation. Surgery is generally required for thoracic perforations while cervical perforations can often
be managed conservatively with continuous nasogastric suction, intravenous broad-spectrum
antibiotics, and parenteral nutrition. Patients with abscesses and effusions require drainage. There has
been a case report of a patient who developed Boerhaave’s syndrome following colonoscopy
preparation due to vomiting. Our patient did not develop vomiting due to the preparation, but did
develop esophageal perforation after colonoscopy.
161
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Annia M Martial, MD
Beware of the “SPICE” you get on street
First Author: A.M. Martial, MD, C. Shaw M.D, H.S. Chitta M.D, H. Moole M.D, S. Bansal M.D.
Synthetic cannabinoids are one of the popular “smokable herbs” today, being marketed as “Spice”,
“K2”. These recreational substances have been shown as the possible cause of biopsy proven Acute
tubular necrosis (ATN) in recent case reports, but the mechanism of action remains unknown. The
unexplained toxicology profile of these drugs along with recent increase in the number of Emergency
room visits from K2 use has created increased concern, both for the extended adverse effect profile and
health care costs incurred. Further, the endless availability, social perception of being safe and the lack
of standardized means of testing has further made it difficult for its identification.
We present case reports of two patients with ATN secondary to synthetic marijuana abuse. Our first
patient was a 29 year old male who presented with confusion and agitation. Laboratory work on
admission showed anion gap lactic acidosis, normal creatinine phophokinase (CPK) levels and a serum
creatinine (SCr) of 1.41. His urine drug screen was positive for Cannabinoids and patient admitted also
to using large amounts of synthetic marijuana. Supportive management with intravenous fluids was
initiated for pre-renal acute kidney injury. Over the next three days, his renal function worsened with
oliguria and a SCr rise to 5.83, suggesting ATN. Our next patient was a young 20 year old male with
polysubstance abuse, who was admitted after he was witnessed to have multiple episodes of
generalized tonic clonic seizures. He was intubated for airway protection and additional work up showed
aspiration pneumonia, anion gap acidosis and acute kidney injury with SCr of 1.6 mg/dl. Despite
adequate hydration, his renal function deteriorated with non oliguric ATN and gradual rise in SCr to 6.77
in four days. After extubation, patient admitted to using synthetic marijuana. Over the hospital course,
his renal function improved without needing renal replacement therapy.
[Date]
In light of the extensive abuse potential and overt neuropsychiatric manifestations of K2, they were
declared as Schedule I control substances by DEA in 2010. They act by binding to the cannabinoid
receptors, CB1 and CB2 similar to marijuana, but differ in being more potent, undetected by routine
testing and easily accessible to teenagers and young adults. The adverse effects include nephrotoxicity,
hypertension, neurotoxicity, respiratory failure, seizures and many more. It is important that physicians
be aware of this phenomenon with K2 use. This knowledge will decrease unnecessary diagnostic testing
as well as expedite focused management. We also suggest that laws be implemented more efficiently
for regulating access to these agents.
162
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Jorge Morales, MD
A rare but life-threatening complication of warfarin therapy: a case of diffuse
alveolar hemorrhage.
Morales, J Nevares, A Nunez, R. Department of Medicine, John H. Stroger, Jr. Hospital of Cook County.
Introduction: Diffuse alveolar hemorrhage is a rare but potentially fatal complication of warfarin
therapy. A high index of suspicion and early diagnosis can be lifesaving.
Case Description: A 77 year old lady presented to our institution referred by her primary care physician
for evaluation of hypoxia and shortness of breath. She complained of three days of worsening dyspnea
on exertion, limiting her exercise tolerance to a few steps. There was no orthopnea, paroxysmal
nocturnal dyspnea, cough or fever. She reported a recent admission elsewhere two weeks prior for
asthma, and discharged on warfarin for newly diagnosed atrial fibrillation. Other past medical history
included hypertension, diabetes and breast cancer in remission. She denied alcohol, smoking or drug
use, but reported exposure to biomass smoke (wood stove) for 16 years before moving from Belize. Her
medications included hydrochlorothiazide, carvedilol, albuterol and beclomethasone inhalers, and
warfarin. Upon presentation, her vitals were: temperature of 98.9°F, pulse rate 103 beats/min,
respiratory rate of 20/min and oxygen saturation of 93% on room air. Cardiopulmonary exam was
remarkable for an irregularly irregular rhythm, bilateral basal crackles and bilateral ankle pitting edema.
Laboratory investigations revealed an initially normal complete blood count with subsequent fall in
hemoglobin but otherwise normal basic metabolic panel. Venous blood gas revealed chronic respiratory
acidosis. International normalized ratio (INR) was 4.71. Chest radiograph showed bilateral alveolar
infiltrates. High-resolution computerized tomography (CT) revealed diffuse groundglass nodular
densities. Bronchoscopy with serial bronchoalveolar lavage (BAL) confirmed alveolar hemorrhage.
Autoimmune workup was negative. Warfarin was held, with complete symptoms resolution at two
weeks follow up.
[Date]
Discussion: Diffuse alveolar hemorrhage (DAH) is most commonly caused by pulmonary capillaritis due
to vasculitis, connective tissue disease and drugs. Warfarin-induced DAH is a rare but potentially fatal
event, with 7 cases reported in the literature since its first description in 1965 by Brown et al. It can
occur early after initiation of therapy and within therapeutic levels of INR. In general, the diagnosis of
DAH requires a high index of suspicion in the occurrence of dyspnea, cough, new alveolar infiltrates and
anemia. If present, a falling hemoglobin supports the diagnosis. Like our patient, hemoptysis can be
remarkably absent in as many as one third of patients and its absence does not rule out the diagnosis.
Serial BALs are usually diagnostic when demonstrating persistent or increasing number of red blood
cells. Underlying “pulmonary-limited” anti-GBM antibody and p-ANCA disease should be considered and
tested, even in the absence of systemic findings. Prompt diagnosis and reversal of coagulopathy are
paramount.
163
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Aswin Nukala, MD
Tumor Lysis Syndrome as a Complication of Chemoembolization with Irinotecan in
a Patient with Primary Colonic Adenocarcinoma with Liver Metastases
First Author: Aswin Nukala, MD Second Author: Jennifer Henson, MBA Third Author: Harish Patlolla, MD
Fourth Author: Pam Khosla, MD
Tumor lysis syndrome (TLS) is a potentially life threatening oncologic emergency resulting from the rapid
lysis of malignant cells in response to chemotherapy or radiation. The rapid lysis of the cells releases the
intracellular contents into the systemic circulation resulting in hyperkalemia, hyperphosphatemia,
hyperuricemia, elevated lactic acid and hypocalcemia. The electrolyte imbalances can result in life
threatening cardiac arrhythmias, seizures, and acute renal failure. The kidneys ability to maintain
acid/base equilibrium is impaired precipitating a severe metabolic acidosis.
TLS is most often associated with hematologic malignancies that have a high turnover rate such as
leukemias and lymphomas. TLS has been rarely reported following cancer treatments directed towards
solid tumors. Based on literature review, since 1977, just 6 cases have been reported of TLS resulting
from colorectal cancer. Only one of these patients survived. To the best of our knowledge, we report
one of the only cases of TLS presenting in a patient with primary colorectal adenocarcinoma with
hepatic metastasis that were directly targeted with trancatheter arterial chemoembolization (TACE)
using Irinotecan drug eluting beads.
Transcatheter arterial chemoembolization of colorectal liver metastasis with Irinotecan has been
described as a novel alternative for patients who have failed attempts at systemic chemotherapy and
who are not surgical candidates. In one review of the safety and efficacy of transarterial
chemoembolization of colorectal hepatic metastases treated with Irinotecan, a total of 57 embolization
sessions were performed with no reports of TLS. Based on our case report, it is evident that Irinotecan,
when targeted directly at tumors, has the capacity, although rare, to rapidly debulk tumor burden and
result in cytolysis and TLS. Prompt diagnosis is important as well as aggressive IV hydration and possibly
emergent dialysis. It is important to know that TLS can be prevented by pretreating certain high risk
cancer patients with fluids and allopurinol prior to receiving chemotherapy.
[Date]
A 68 yo female with past medical history of primary colonic adenocarcinoma with known hepatic
metastases presented to the emergency room complaining of generalized fatigue, diffuse abdominal
pain, watery, non bloody diarrhea, and multiple episodes of nonbloody, non bilious vomiting of 5 days
duration. The patient was being treated with outpatient chemotherapy with FOLFIRI with cetuximab.
Seven days prior, she received chemoembolization with irinotecan directed at her hepatic metastases.
The patient was hemodynamically stable on admission, although she was found to have severe
electrolyte derangement, including hyperkalemia, hyperuricemia, and hyperphosphatemia and she was
in Acute Renal Failure. Blood gas analysis showed severe metabolic acidosis, with elevated lactate. The
patient was subsequently admitted to the Medical ICU with a diagnosis of TLS following
chemoembolization. She received aggressive fluid hydration, emergent dialysis, and was given
allopurinol/rasburicase. She responded very well and was discharged home the following week.
164
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Aswin Nukala, MD
An Unusual Case of Hepatitis C Associated Cryoglobulinemia and
Membranoproliferative Glomerulonephritis Presenting as Diffuse Alveolar
Hemorrhage
First Author: Aswin Nukala, MD Second Author: Aravindan Jeyarjasingam, MD Third Author: Andres
Serrano, MD
Cryoglobulinemia is a rare condition in which immunoglobulin and complement complexes precipitate in
the blood at temperatures colder than 37 degrees Celsius. The formation of these immune complexes
leads to deposition in capillaries and small arterioles resulting in a systemic vasculitis that can present as
palpable purpura, neuropathy, arthralgias and myaligias, renal and/or liver failure.
Membranoproliferative glomerulonephritis (MPGN) is a frequent finding due to deposition of immune
complexes of the hepatitis C virus, IgG, and IgM rheumatoid factors. The lungs, if involved, usually
demonstrate a restrictive pattern in which there is an impairment of gas exchange. However,
pulmonary vasculitis and resulting hemorrhage is an extremely unusual entity. In this case, the authors
describe a rare presentation of hepatitis C associated mixed cryoglobulinemia and
membranoproliferative glomerulonephritis (MPGN) resulting in diffuse alveolar hemorrhage.
A 63 year old Hispanic male with a history of IV heroin abuse, Hepatitis C associated mixed
cryoglobulinemia (Type 2) and MPGN presented to the emergency room with complaints of worsening
dyspnea and hemoptysis with streaks of blood for the past 2 weeks. A basic metabolic profile revealed
that the patient had an acute kidney injury with an elevated creatinine of 2.9, which was above his
baseline of 1.9. A chest X ray revealed diffuse alveolar infiltrates. A CT of his chest revealed diffuse
ground glass opacities in the lung apices and bilateral pleural effusions. Cryoglobulin and hepatitis C
antibody were also positive, with viral load greater than 7 million. Complement levels were decreased
and rheumatoid factor was elevated at 122 (<14 IU/ml). ANCA related vasculitis was ruled out. The
patient underwent bronchoscopy, which revealed an erythematous airway and grossly bloody
fluid. Analysis of the BAL revealed greater than 31,000 RBC’s confirming the suspected diagnosis of
alveolar hemorrhage. Because of the renal and pulmonary involvement of the underlying
cryoglobulinemia, the patient was treated with plasmapheresis and rituximab and improved clinically.
[Date]
Alveolar vasculitis has been very rarely described as a presentation of cryoglobulinemia. Although
numerous pulmonary renal syndromes have been reported, it is an extremely rare entity for
cryoglobulinemic MPGN to present in such a way. Through literature review, there appears to be no
more than fifteen such cases reported. The pathophysiology likely involves immune complex deposition
in the small capillaries of the airway. In this case we highlight the importance of early diagnosis to detect
acute renal failure, management of the airway in a patient with active hemoptysis, and laboratory
testing to determine whether the patient will benefit from plasmapheresis, corticosteroids, and/or
immunosuppressive therapy. Even with successful treatment of acute flare-ups, pulmonary involvement
in patients with cryoglobulinemia portends a very poor overall prognosis.
165
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Chibuzo C Odigwe, MD
Richter’s Transformation of Chronic Lymphocytic Leukemia to Classical Hodgkin
Lymphoma
First Author: Chibuzo C Odigwe, MD John I Ngene, M Waqar, C Ghobadi, K Kozma, K Maliekel and A
Gilman
A feared complication of Chronic Lymphocytic Leukemia (CLL) and Small Cell Lymphocytic Lymphoma
(SLL) is Richter’s transformation. It occurs in 5% of cases and is the progression of an indolent leukemia
to an aggressive high-grade large cell lymphoma. In rare cases CLL may transform into classical Hodgkin
Lymphoma (HL). Less than one hundred cases have been documented to date.
We report the case of an 88 year old lady admitted to our hospital following worsening fatigue, anorexia
and syncope. Prior to admission she received Rituximab and three cycles of Bendamustine with minimal
response. Physical examination revealed pallor, cachexia and a right sided scalp laceration. CT of the
head showed acute on chronic bilateral subdural hematomas with a depressed skull fracture.
Her hospital course was significant for low-grade fevers and persistent lymphocytic leukocytosis. She
had marked anemia and thrombocytopenia refractory to transfusions even after pre-treatment with IV
dexamethasone and IV immunoglobulin. Work up for infectious etiology and autoimmune hemolysis
was negative. Hematologic evaluation revealed a reticulocyte count of 2.5 (index of 0.6). CT scan of the
abdomen and pelvis revealed marked splenomegaly and retroperitoneal lymphadenopathy with interval
worsening. She underwent a bone marrow biopsy which showed two separate abnormal cell infiltrates.
The first was comprised of large abnormal lymphoid cells with multiple lobulated nuclei and prominent
nucleoli consistent with Reed Sternberg (RS) cells, supporting a diagnosis of classical HL with 30% bone
marrow involvement. Immunohistochemical staining was positive for PAX 5, CD30 and negative for
CD20. The second infiltrate was consistent with her prior diagnosis of CLL with 50% bone marrow
involvement.
[Date]
Richter’s transformation portends a poor prognosis in the clinical course of CLL/SLL. It should be on the
radar whenever a patient begins to deteriorate with refractory cytopenia. The MD Anderson Cancer
Center published a series of 4,121 patients with CLL/SLL, identifying only eighteen patients (0.4%) with
transformation to HL. Richter’s transformation to HL can be classified into two types. Type 1 is
illustrated by RS cells scattered in a background of CLL cells, whereas Type 2 is illustrated by RS cells
within a typical polymorphous, inflammatory background separate from CLL cells. Our case most closely
represents a Type 1 pattern. In the MD Anderson series, median survival for Type 1 transformation was
0.8 years. Our patient received treatment with Chlorambucil, Procarbazine and Prednisone/Solucortef
and was transitioned to hospice after the first cycle. More aggressive approaches include therapeutic
regimens such as Lomustine, Mitoxantrone, Vinblastine combination, the Stanford V regimen followed
by radiotherapy and MOPP/ABVD. We opted for a more conservative approached in view of her overall
performance status.
166
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Venu Pararath Gopalakrishnan, MD
Can a Verse (POEM) get any worse!?
First Author: Venu Pararath Gopalakrishnan, MD 1 Second Author: Malav P Parikh, MD 1 Third Author:
Sreelakshmi Panginikkod , MBBS 2 Fourth Author: Chandramohan Meenakshisundaram, MD 1
Institutional Affliations: 1)Department of Internal Medicine, Presen
Introduction: POEMS syndrome is a rare paraneoplastic syndrome resulting from underlying plasma cell
disorder. The acronym represents several of the defining features which includes
Polyradiculoneuropathy, Organomegaly, Endocrinopathy, Monoclonal plasma cell disorder and Skin
changes. The patients also have features of extravascular volume overload which can manifest as
peripheral edema, pleural effusion, pericardial effusion and ascites which is believed to be from
increased vascular permeability due to excess vascular endothelial growth factor (VEGF) activity. Early
diagnosis and a prompt multidisciplinary approach increase the likelihood of reduced long-term
morbidity and mortality.
Case Presentation: A 52 year old male presented with insidious onset of abdominal distention for the
past two months. His past medical history was significant for hypothyroidism and sensory motor
polyneuropathy diagnosed five years ago. Physical examination revealed a cachectic male with
hyperpigmentation, sclerodermoid skin changes, significant ascites and mild pedal edema. Laboratory
studies revealed normal liver function tests with albumin of 4.3 mg/dl and international normalized ratio
(INR) of 1.1. Hepatitis and HIV serologies were non-reactive. CA-125 and CEA levels were within normal
limits. Ascitic fluid analysis revealed a serum ascites albumin gradient (SAAG) of 0.9 gm/dl and ascitic
fluid protein of 3.2 gm/dl. Chest x-ray showed a normal sized heart with mild right pleural effusion.
Transthoracic echocardiogram showed normal right and left ventricular function with ejection fraction
of 62%. Computerized tomography (CT) scan of the abdomen showed normal liver, massive amount of
ascites, splenomegaly and retroperitoneal lymphadenopathy. Serum protein electrophoresis (SPEP)
showed an M spike and serum Immunofixation was consistent with IgA lambda monoclonal
gammopathy. Serum VEGF and IL-6 levels were elevated. Based on the overall clinical picture and
investigations, the patient was diagnosed with POEMS syndrome. The patient was started on melphalan
and dexamethasone and showed significant clinical improvement in the follow up period.
[Date]
Discussion: POEMS syndrome is a rare paraneoplastic syndrome which is caused by an underlying
plasma cell disorder. Apart from the characteristic features of POEMS syndrome, patients also have
extravascular fluid overload which most commonly manifests as peripheral edema, but pleural effusion
and ascites are also common. Ascites may be severe enough to require weekly paracentesis. Patients
have a low serum-ascites albumin gradient (SAAG) in the ascitc fluid, consistent with an exudative
process rather than a portal hypertension process. There is no standard treatment for POEMS syndrome
and no randomized controlled trials of treatment exist in the available literature. Systemic
chemotherapy with the use of melphalan plus dexamethasone has demonstrated good response rates
with an acceptable toxicity profile Ascites often responds to the administration of diuretics, but may
require drainage with paracentesis. Median survival in patients of POEMS syndrome with extravascular
fluid overload was determined to be 6.6 years.
167
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Siwadon Pitukweerakul, MD
Acute pericarditis as a rare consequence of Severe Diabetic Ketoacidosis
First Author: Siwadon Pitukweerakul, MD
DKA is a medical emergency in DM type 1 patients which may result in severe complications if not
treated effectively. Acute Pericarditis was described as one of the very rare complications of DKA
which is uncommon in mild to moderate DKA but has been reported in severe cases of DKA. The
following report is a case of acute pericarditis that developed while treating a patient with severe
diabetic ketoacidosis.
A 33-year-old Hispanic man with insulin-dependent diabetes of 15 years' duration was admitted to the
hospital with a 2-day history of nausea, vomiting, and worsening shortness of breath. He endorsed loss
of appetite and was unable to hold food down. He vomited a number of times after attempts to drink
soup. There were no changes in urinary frequency. He decided to stop taking insulin yesterday because
of poor oral intake. He stated that he had been compliant to his insulin until yesterday. His normal
insulin regimine includes lispro 15 units before meals , and glargine 20 units at bedtime. He denied any
chest pain, palpitations, fever, cough, and heat or cold intolerance. On examination he was alert and
oriented to person, place, and time. He was found to have had Kussmaul's respirations. The
temperature was 35.3°C, pulse 135/minute,and blood pressure 118/58 mmHg. Auscultation of the heart
and lungs was normal. The abdomen was soft and bowel sounds were present. Initial labs showed a
blood glucose of 900 mg/dL, plasma bicarbonate 3 mmol/L, blood urea 33 mg/dL, plasma sodium 133
mmol/L, potassium 5.7 mmol/L, with a calculated serum osmolality of 299 mosmol/kg. There was no
evidence of any precipitating infection on history. Blood cultures, throat swab for viral infections, and
urine culture were all sterile. He was diagnosed with severe DKA and was treated with intravenous
fluids and insulin infusion. After 48 hours of hospitalization, he began to complain of substernal chest
pain. This pain was very sharp in character, worse on deep inspiration. Electrocardiogram was done and
shown definite ST elevation in leads I-III,AVL,AVF and V2-V6. Troponin T was elevated to 29
ng/mL from 0.01 on admission. The Echocardiogram showed normal left ventricular size and
contractility with LVEF 63%. He was diagnosed with acute pericarditis and given aspirin. He showed
improvement clinically. He denied pleuritic chest pain 1 day after aspirin was started. He was discharged
home 5 days after admission
[Date]
This case illustrates a rare complication of diabetic ketoacidosis. Although most cases of acute
pericarditis are not life-threatening and considered a benign condition, it is important for clinicians to
recognize this complication, so that they can provide appropriate treatment for their patients.
168
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Siwadon Pitukweerakul, MD
What we have learned from lithium toxicity.
First Author: Siwadon Pitukweerakul, MD Pakhadi Buddhadev , MD
Lithium toxicity may be acute, such as a patient who is not on lithium therapy that ingested a bottle of
lithium tablets in a suicide attempt; acute-on-chronic, such as a patient who is on lithium therapy that
also ingested a large number of lithium tablets all at once; or chronic, which commonly presents as
patient on a stable lithium regimen that suffers a reduction in renal function. Poly-pharmacy is also
known to increase the risk of developing lithium toxicity.
A 44 year-old woman with a past medical history of DM type 2, HTN, depression, bipolar disorder type 1,
and epilepsy presented to Emergency Department with dizziness and confusion in this morning. She fell
down and hit her head, but did not have obvious external bleeding. She denied chest pain palpitations,
numbness, weakness, visual changes, sweating, loss of consciousness, fever, burning urination, or
abdominal pain. She also reported the associated symptoms of nausea and 2 episodes of vomiting.
According to her fiancé, the patient was completely normal yesterday evening. On the morning of
admission, the patient was not her usual self. She seemed drowsy and confused. When asking about
medication, the patient reported that she takes her meds regularly. The medications include: fluoxetine,
gabapentin, lisinopril, lamotrigine, olanzapine, lithium, metformin and sitagliptan. She has had back pain
lately and had also been taking ibuprofen over the counter 6-10 tablets a day for 3 days. Physical exam
was unremarkable except for resting and action tremor in both hands. She remained drowsy but was
easily aroused on the floor and she remained oriented to time, place and person. Diagnostic work up
found a creatinine level elevated to 5.86 mg/dl (last known Cr. was 0.6 mg/dl 2 years ago), arterial Blood
gas Shows Normal-gap metabolic acidosis(pH 7.16,pCO2 31, pO2 122, HCO3 11) and a lithium level of
2.5 mmol/L (N=0.5-1.3 mmol/L). On the day following admission, the patient was intubated because of
shortness of breath and flash pulmonary edema. She received emergent hemodialysis and her lithium
level decreased from 2.5 to 0.9. She was also diuresed with furosemide. Her creatinine improved to
0.89. She was extubated 7 days later.
[Date]
This case illustrates the value of a complete history. It is important that clinicians be aware of the risk
factors for developing lithium toxicity. Medications that cause dehydration or renal impairment can
precipitate lithium toxicity because lithium is excreted almost entirely by the kidneys. In this case,
patient took high dose of new medication, ibuprofen, which was nephrotoxic given she was already
taking lisinopril. Moreover, AKI was likely the cause of the patient’s lithium toxicity. Therefore, this case
emphasizes the importance of inquiry concerning new medications or changes in the doses of longstanding medications.
169
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Moni Roy, MD
Carbapenem Resistant Aeromonas Caviae Causing Infected Pancreatic Pseudocyst
Moni Roy, MD., Vijaya Somaraju, MD., Department of Internal Medicine, University of Illinois college of
Medicine, Peoria, Illinois.
Introduction: Aeromonas bacteria is widely distributed in the environment and usually sensitive for
carbapenems. Resistance of carbapenems in Aeromonas species is rare. Resistance is usually mediated
by chromosomal cphA gene. Here is a rare case of Meropenem resistant Aeromonas caviae associated
with necrotizing pancreatitis.
Case: A 50 year old male, with intellectual disability, living in group home presented with abdominal
pain and watery diarrhea. His evaluation revealed elevated lipase, Ultrasound showed CBD dilatation
and gall bladder thickening. Pt was placed on symptomatic care for acute pancreatitis with IV fluids, pain
management. During course of hospitalization patient had intermittent low grade fevers, spiked
temperature upto 101.4 and abdominal symptoms of diarrhea and pain persisted. Patient was started
on Meropenem. CT abdomen on day 8 was consistent with necrotizing pancreatitis and with large
pseudocyst measuring 14.1 x 6.6 cm. A CT guided pseudocyst aspiration and percutaneous drain was
placed by Interventional Radiology. Aspiration cultures reported for heavy growth of Aeromonas Caviae
resistant to Meropenem and Piperacillin-Tazobactam but susceptible to other antibiotics on the panel.
Antibiotic coverage was changed to Fluoroquinolones and with change in coverage patient’s fevers,
leukocytosis and diarrhea gradually improved. Follow up CT on Day 15 showed interval drainage of fluid
collection anterior to the pancreas. Antibiotics continued for few more days and patient was discharged
in stable condition.
[Date]
Discussion: Aeromonas species are globally distributed Gram-negative, oxidase-positive rods, found in
aquatic environments, foods, and the microflora of fish. Though GI tract is by far the most common site
from which the bacteria is recovered, its role as etiologic agent for gastroenteritis has not been
established. No animal model has been established that can reproduce Aeromonas associated diarrhea.
Infection may be acquired in humans by drinking contaminated water, ingestion of sufficient number of
organism in contaminated food or through open wounds. Aeromonas has been associated with few
outbreaks of diarrhea in long term care facilities which may be related to sub optimal hygienic
conditions. Aeromonas has been shown to be a significant cause of infections after natural disasters.
Most Aeromonas species are Meropenem sensitive. Very few cases of Carbapenem resistance have
been reported. Aeromonas infection has been associated with serious conditions such as Cholangitis and
HUS. Most hepatobiliary infections have been in cases with underling malignancy or
immunosuppression, usually in patients with biliary tract obstruction. The case above did have biliary
tract obstruction, and gall stone pancreatitis complicated with severe necrotizing pancreatitis and
Aeromonas infected pseudocyst.
170
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Dhavel Save, MD
Alcoholic intoxication leading to Rhabdomyolysis and Bilateral Sub-massive
Pulmonary Embolism
First Author: Dhavel Save, MD Second Author: Joshua Baru, MD
Introduction: Venous Thromboembolism is an uncommon but potentially lethal event in acute alcohol
intoxication complicated by Rhabdomyolysis.
Case: 27 year old Indian man with no past medical history brought to the Emergency Department
unresponsive for an unknown period of time. Upon arousal he admitted drinking a bottle of vodka.
Physical examination was pertinent for respiratory rate of 24/min, Heart Rate of 130/min, dry mucosa
and alcoholic smell of breath. Labs were significant for potassium of 5.1 milliequivalents/Liter, Lactic
acidosis with anion gap of 21, transaminitis, Increased Lactate Dehydrogenase (LDH) of 899 and a Blood
alcohol level of 330. Other toxicology was negative. Urine dip stick showed large blood but urinalysis
showed only one RBC. Creatinine Kinase levels were 21605. A diagnosis of Rhabdomyolysis was made.
While in the Emergency room, Patient became tachypneic, tachycardic and hypoxemic with oxygen
saturation dropping to 80’s on room air. A Computed Tomographic (CT) Angiogram of the chest was
performed and showed bilateral pulmonary embolism with evolving pulmonary infarcts. Bedside Transthoracic 2-Dimensional Echocardiogram showed severe Right Ventricular dilatation with hypokinesia
and preserved Left ventricular function. Troponin-I was elevated to 0.68. Ultrasound (US) Doppler of
lower extremities was negative for thrombus. Anti-thrombin III, Protein C, Protein S deficiency, Factor 5
Leiden, homocysteinemia was ruled out with negative Laboratory tests. Patient was started with anticoagulation with Heparin infusion and was admitted to Medical Intensive care unit (MICU) for
observation He stabilized within hours and was eventually discharged home with Low molecular weight
heparin bridged with Warfarin therapy.
[Date]
Discussion: The majority of cases of Rhabdomyolysis are non-traumatic, and alcohol abuse is one of the
most common causes. The short term alcohol intoxication, immobilization or coma induced by ethanolrelated central nervous system sedation plays an important role in developing Rhabdomyolysis. It causes
muscle compression and muscular ischemia, which superimposes or accelerates short-term alcohol
myotoxicity, resulting in a massive breakdown of skeletal muscle within a short period. This leads to
rapid release of osmotically active agents into the interstitial space and rapid increase of compartmental
pressure and can even cause a compartment syndrome. Because of rapid release of muscle cell contents
from damaged muscle into circulation, which include tissue thromboplastin and other pro-thrombotic
substances, Rhabdomyolysis is a hyper-coagulable state and these patients are at risk of developing
Thrombosis. There is also increased factor VIII pro-coagulant protein in muscle breakdown which may be
a predisposing factor for DVT. These patients are also likely to be complicated with hyperkalemia,
metabolic acidosis, acute renal failure, multi-organ failure, or disseminated intravascular coagulation.
Although there are case reports in literature of development of Rhabdomyolysis following acute alcohol
intoxication, development of bilateral sub-massive pulmonary embolism is rare and makes this case an
interesting clinical vignette.
171
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Anushi Shah, MD
A Perplexing Cause of Acute Renal Failure in Prostate Cancer
First Author: Anushi Shah, MD Teresa Lynch, MD, Dilini Reyhart, MD.
An 86 year old male with metastatic prostate cancer post retropubic radical prostatectomy in 1993 and
stage 3 chronic kidney disease (baseline creatinine 1.9) was transferred for evaluation of acute renal
failure with concern for urosepsis and adrenal crisis. He had a 1 week history of anuria and increased
pelvic pain resulting in a recent hospital admission for opioid overdose. Pertinent positives on review of
systems included penile pain and edema, dysuria, and fevers. Of note, abiraterone acetate and
prednisone had been initiated 2 months prior to admission for metastatic disease. On physical exam he
was hypotensive, tachycardic, and afebrile. He had significant penile and scrotal edema with dry blood
surrounding the urethral meatus. Admission labs showed PSA>2000, hyponatremia (132), hyperkalemia
(6.9), hypocalcemia (7.3), BUN 47, creatinine 4.10, AST 272 and ALT 95. CBC demonstrated leukocytosis
(23) with neutrophilia (75). Urological consultation was required for cystoscopic urethral calibration and
foley insertion. Renal ultrasound demonstrated extensive hepatic hyper-echoic nodules consistent with
known metastases. On day 2, urine culture resulted positive for enterococcus, treated with Augmentin.
Although renal function and hemodynamic status improved with these measures, his calcium continued
to trend down, and by day 3, reached a critical level of 5.0. The hypocalcemia was presumed to be
secondary to hyperphosphatemia (6.8) secondary to AKI, but further work up revealed that in addition
to hyperparathyroidism (523), the patient also had an LDH of 9725 and uric acid of 13.7. The diagnosis
shifted to tumor lysis syndrome with the high tumor load indicated by PSA>2000 (versus 500 prior to
initiating therapy), rising alkaline phosphatase, and correlating findings on abdominal ultrasound
demonstrating innumerable liver metastases. Nephrology initiated febuxostat, calcium acetate, vitamin
D, and IV bicarbonate/D5W, resulting in a drop in LDH to 5037, uric acid to 10.2, and increase in calcium
to 6.3 (7.2 corrected). The patient then requested no further intervention and was discharged on
allopurinol on day 5.
[Date]
Tumor lysis syndrome is an oncological emergency resulting in massive derangement of electrolytes and
organic acids predisposing to arrhythmias and renal failure. It is most commonly seen with aggressive
hematological malignancies and very rarely associated with solid tumors. Of these, prostate cancer is
even less commonly implicated. Although limited reports of TLS following treatment with docetaxel and
paclitaxel for prostate cancer exist, there are zero cases reported while on abiraterone therapy. A low
index of suspicion for TLS caused our patient’s symptoms to be attributed to other confounding
variables, leading to a delay in diagnosis and appropriate management. In the case of high tumor
burden, regardless of tumor type, a high index of suspicion must remain for tumor lysis syndrome.
172
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Timothy Shih, DO
Sweetheart: A Case of Tricuspid Valve Endocarditis Presenting as Hyperosmolar
Hyperglycemic State (HHS)
First Author: Timothy Shih, DO MS
Infective endocarditis is a disease characterized by inflammation of the endocardium, most commonly
of the heart valves. It prototypically presents with a vegetation, a mass consisting of platelets, fibrin,
microorganisms, and inflammatory cells. The disease was first described in the mid 16th century, but
despite significant advances in diagnosis and treatment the morbidity and mortality remain
high. Infective endocarditis has been associated with a number of complications including stroke and
thromboembolic phenomena, heart failure, and intracardiac abscess formation. Diagnosis can be a
challenge as many of the clinical findings are subtle and nonspecific. However, careful history and
physical examination, serologic testing, and imaging can assist in making the correct diagnosis.
This case highlights the oftentimes challenging nature of obtaining a definitive diagnosis for infective
endocarditis. Despite the initial negative echocardiography, the patient was treated for presumptive
infectious endocarditis based on high clinical suspicion. Interestingly, the patient developed right sided
endocarditis despite having no known risk factors, e.g. drug use or structural heart defects. The
patient’s presentation, however, was fairly typical of right sided endocarditis, where septic pulmonary
emboli are more common than the more easily visible peripheral embolic phenomena such as splinter
hemorrhages, Janeway Lesions, and Osler Nodes. Despite his complicated hospital course, the patient
was fortunate in that he had no permanent valvular dysfunction necessitating surgical intervention. The
initial presentation in this case demonstrates how the severity of underlying infection can expose
undiagnosed diabetes, which furthermore highlights the importance of persistence in searching for
underlying disorders in the setting of high clinical suspicion.
[Date]
Mr. G is a 45 year old male with no previous known past medical history who presented with weakness
and a serum glucose of 728 without evidence of metabolic acidosis or ketonuria concerning for
HHS. While his HHS was being appropriately treated with an insulin drip, initial workup for an
underlying infectious etiology was notable for a leukocytosis to 18,000 as well as blood and urine
cultures positive for gram positive cocci. Accordingly, the patient was started on IV vancomycin. Later
on, the cultures resulted in pan-sensitive staph aureus, and the vancomycin was changed to IV
nafcillin. Although the patient was initially afebrile, he began experiencing fevers on hospital day 5. To
assess for the source of bacteremia, a CT of the chest was done which showed multiple peripheral
pulmonary nodules suspicious for septic emboli. A TTE and TEE were performed and both were negative
for vegetations. The patient continued to have fevers despite appropriate treatment with nafcillin, and
so a repeat TTE was performed which revealed a small mobile echodensity seen on the tricuspid
valve. The patient was continued on IV nafcillin, however he developed renal dysfunction which was
concerning for interstitial nephritis, and his antibiotic was switched to IV cefazolin. The patient
improved on cefazolin, which was continued for a total of 6 weeks. Mr. G was discharged with follow up
with his PCP and with endocrine clinic for his newly diagnosed diabetes. A repeat TTE 4 months later
showed only trivial tricuspid regurgitation and no signs of the previously seen vegetation.
173
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Nabeel H Siddiqui, MD
May-Thurner Syndrome: A rare cause of Deep Venous Thrombosis
First Author: Nabeel H Siddiqui, MD
May-Thurner Syndrome is a rare cause of Deep Venous Thrombosis (DVT), and one that can be missed
easily. Herein, we report a case of May-Thurner Syndrome in a young female.
Case: A 20-year-old female presented to the hospital with left lower extremity pain and swelling for one
week. The swelling was initially in her foot and traveled up to her thigh, and the pain made her unable
to ambulate. She denied any recent immobilization, travel or limb trauma. She reported oral
contraceptive use and history of smoking one cigarette daily each for the past one year. She denied any
history of blood clots. Her family history was insignificant. She had stable vital signs. On exam, she had
unilateral pitting edema in her left lower extremity up to the thigh, and tenderness to palpation in left
posterior leg. D-Dimer was elevated at 7.2. Her coagulation profile and other tests for hereditary
thrombotic disorders were normal. Ultrasound venous duplex identified a blood clot from the calf
extending cephalad proximal to the femoral head, confirming the presence of DVT. She was started on
anticoagulation with therapeutic enoxaparin. To prevent clot embolization, inferior vena cava filter (IVC)
was placed. Moreover, as no clinical improvement was observed, tissue plasminogen activator was
infused through a catheter in the left iliac vein. However, her pain persisted. Repeat CT angiogram
showed extensive thrombus within the left common iliac vein, left external iliac vein and left femoral
vein. There was also noticed to be narrowing in the distal aspect of left common iliac vein, secondary to
compression from a crossing left common iliac artery. This suggested the diagnosis of a variant of MayThurner Syndrome. She underwent placement of stents in left common iliac vein and left iliac vein at
level of pelvic rim. Eventually, her symptoms of pain and swelling resolved with the preceding
interventions. Her IVC filter was removed, and she was discharged in a stable condition on warfarin with
follow up arranged with her hematologist.
Discussion: May–Thurner syndrome is a rare condition usually involving compression of the left
common iliac vein by the overlying right common iliac artery, however, other variants like the one in our
patient also exist. This can result in stasis of blood, leading to thrombosis.
Vascular ultrasound or CT angiogram are used to establish the diagnosis. Treatment is based on
angioplasty and stenting of iliac vein.
[Date]
Our case demonstrates that one should consider rare causes of DVT such as May-Thurner syndrome in
young patients with no other identifiable causes. Thorough investigation and imaging can help identify
the condition, and hence, prevent re-thrombosis in such patients.
174
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Simranjit Singh, MD
Lung Hamartoma. Is it really a benign pathology?
Simranjit Singh, MD Fnu Sanna, MD Sujay Bangarulingam, MD
Introduction: Pulmonary hamartomas are the most common benign tumor-like lesions of the lung.
Mostly found incidentally on routine imaging, they constitute 5-8% of all solitary pulmonary nodules.
They arise as an outgrowth from epithelial lung elements and normal mesenchymal tissue of the lung.
Ewing’s sarcoma (ES) and peripheral primitive neuroectodermal tumor (PNET) are part of a spectrum of
neoplastic diseases known as the Ewing’s sarcoma family of tumors (EFT). It also includes extraskeletal
Ewing’s sarcoma (EES), which is quite rare and predominantly involves the soft tissues of the trunk or
the extremities. Primary ES of the lung is an extremely rare tumor. We described a case of pulmonary
hamartoma which got converted into a pulmonary primary ES tumor over the course of 7 years. This
case highlights the importance of routine monitoring of lung hamartomas, which as demonstrated in the
present case can convert into a malignant tumor.
Case: A 38-year-old female presented to the clinic with 1 month history of cough, shortness of breath
and dysphagia. She had a history of biopsy proven hamartoma at the right cardiophrenic angle,
diagnosed 7 years ago. Plain chest radiography revealed significant increase in the size of the previously
present mass. Computed tomography (CT) showed a 6 cm x 7 cm x 9 cm soft tissue heterogeneous mass.
Similar location of the mass was confirmed after comparison with the previous imaging studies. CT
guided core biopsy followed by histopathologic and immunohistochemistry studies confirmed the
diagnosis of EES. Positron emission tomography –computed tomography (PET-CT) revealed increased
fluorodeoxyglucose (FDG) uptake by the mass, left lobe of the liver and multiple hyper-metabolic bone
lytic lesions. Considering the metastatic spread of the tumor, the patient was opted for neoadjuvant
chemotherapy followed by the radiotherapy.
[Date]
Discussion: ES is a rare malignant disease which generally involves pediatric population. Only 5% of all
cases occur in adults. Moreover, EES originating in the lung is extremely rare, with less than 15 cases
been reported in the published literature. The present case demonstrates a unique clinical occurrence.
This patient had a biopsy proven lung hamartoma and presented 7 years later with the conversion of the
mass into Ewing sarcoma. ES of the lung is an aggressive tumor and needs multidisciplinary approach.
However, as in the present case, the prognosis remains poor. Hamartomas are considered benign
tumors and no treatment is indicated for asymptomatic lesions. However, radiographic follow up is
recommended for at least 2 years to confirm their benign nature and to establish a growth rate. The
present case underscores the significance of routine monitoring of benign lung neoplasms.
175
ILLINOIS POSTER FINALIST - CLINICAL VIGNETTE Teja V Surapaneni, MD, MS
Diffuse alveolar hemorrhage (DAH) secondary to amiodarone and apixaban use: A
case report
Teja V. Surapaneni MD MS 1, Mina A. Farahani MD MS MS 2, Erica M. Fernandez PharmD BCPS 3 , Kaveh
Tayebi MD 4 1. Second year internal medicine resident physician 2. First year transitional year resident
physician 3. Clinical Pharmacy Specialist 4. Criti
Diffuse alveolar hemorrhage is a clinical syndrome resulting from pulmonary capillaritis, bland
pulmonary hemorrhage, or diffuse alveolar damage.1 DAH has been reported as a rare adverse event
with amiodarone therapy, warfarin therapy, and as a potential complication with rivaroxaban therapy. 2,
3, 4
We present the case of a seventy-six year old Hispanic female with a medical history significant for heart
failure with preserved ejection fraction, obstructive sleep apnea with associated pulmonary
hypertension and right heart strain, type two diabetes mellitus, stage four chronic kidney disease,
gastroesophageal reflux disease, chronic anxiety, dementia, and hypothyroidism who had presented
with complaints of atypical chest pain, shortness of breath, and anxiety. Chest x-ray performed at
admission showed patchy asymmetric infiltrates suggestive of worsening heart failure. The patient was
then aggressively diuresed for pulmonary edema and presumed worsening heart failure. Thereafter, her
hospitalization course was complicated by new onset acute non-valvular atrial fibrillation. Rhythm
control with amiodarone was then initiated. Given her high risk for stroke based on CHADS-VASc score
of six, anticoagulation was initiated with apixaban. Six days later, the patient developed respiratory
failure due to acute respiratory distress syndrome (ARDS) confirmed by extensive bilateral consolidation
on chest x-ray. During intubation, gross blood was noted to be lining the endotracheal tube.
Amiodarone and apixaban were then held due to suspicion for alveolar hemorrhage. Systemic steroids
were also initiated to prevent relapse and extensive continued pulmonary fibrosis. She was maintained
on ventilator support with a strategy to treat underlying ARDS secondary to DAH. After four weeks of
unsuccessful withdrawal of ventilatory support, the patient required tracheostomy and was then
transferred to an inpatient rehabilitation facility.
Amiodarone monotherapy has been associated with DAH, and the concurrent anticoagulant effect of
apixaban may have increased her risk of bleeding. The potential pharmacokinetic drug interaction
between amiodarone and apixaban or the patient's diminished renal function, whether independent or
additive, cannot be excluded as contributing factors in this case of DAH.
4.
Lara A, Schwarz M. Diffuse alveolar hemorrhage. Chest 2010; 137 (5): 1164-71.
Iskandar SB et al. Amiodarone-induced alveolar hemorrhage. South Med J. 2006 Apr;99(4):383-7.
Uysal E, Cevik E, Solak S, Acar Y, Yalimol M. A life-threatening complication of warfarin therapy in ED: diffuse alveolar
hemorrhage. Am J Emerg Med. 2014 Jun; 32(6):690.
Uysal E. 1239: Drowning in blood: a rare but fatal complication of rivaroxaban. Crit Care Med. 2012 40 (12): 1-328.
[Date]
1.
2.
3.
176
INDIANA POSTER FINALIST - CLINICAL VIGNETTE Emily Cochard, MD
Searching for Sarcoid: Utility of PET/CT Scan
First Author: Emily Cochard, MD Additional Authors Ishan Gohil, MS4; Robert J. Fick, MD
Sarcoidosis is an inflammatory, granulomatous disease of unknown etiology. The disease most often
presents with pulmonary symptoms and characteristic radiographic findings of hilar lymphadenopathy.
Isolated extrapulmonary sarcoidosis presents a diagnostic challenge.
A 61 year-old gentleman whose past medical history included atrial fibrillation and type 2 diabetes
mellitus presented with malaise, anorexia, a sixty pound weight loss, mild cognitive changes and
hypercalcemia, 14.1 mg/dL (8.4-10.5 mg/dL). None of his medications were known to cause
hypercalcemia. His exam was unremarkable for lymphadenopathy, pulmonary abnormalities, abdominal
tenderness, hepatosplenomegaly or skin findings. He was started on intravenous normal saline,
furosemide, calcitonin and pamidronate, while workup was initiated. Laboratory data revealed an
appropriately suppressed PTH, normal PTHrp, normal serum and urine protein electrophoresis, normal
urine Ca:Cr ratio, and a normal kappa/lambda light chain ratio. His 1-25 hydroxyvitamin D was 99 pg/mL
(18-72 pg/mL) and his angiotensin converting enzyme level was 99 U/L (9-67 U/L). Skeletal survey was
negative for osteolytic lesions. CT showed multiple <5mm calcified nodules throughout the lungs and
mild splenomegaly, which were not felt to be significant by the consulting pulmonologist. A whole-body
PET/CT was pursued which demonstrated heterogeneous uptake throughout his bone marrow, one
hypermetabolic lymph node in his left neck, and mildly prominent splenic uptake. Bone marrow biopsy
subsequently revealed normocellular bone marrow and the presence of non-caseating granulomas. The
presence of non-caseating granulomas in the bone marrow along with the patient’s clinical presentation
confirmed the diagnosis of isolated extrathoracic sarcoidosis as a very rare etiology of refractory
hypercalcemia.
[Date]
Sarcoidosis primarily involves the lungs and while extrapulmonary sarcoidosis is common (30-50%), it is
usually concomitant with pulmonary involvement. In a study with 736 sarcoidosis patients, 95% had
thoracic involvement, 50% had concomitant extrathoracic disease and only 2% had isolated
extrathoracic sarcoidosis. Hypercalcemia is seen in only 10-20% of all cases of sarcoidosis.
Extrapulmonary disease can be severe and life threatening and its presence can impact the therapeutic
approach. Diagnostic dilemmas arise when trying to search for affected organs, particularly when
patients are asymptomatic. The use of PET/CT relies on glucose hypermetabolism by granuloma cells
and can be used for mapping of inflammatory sites and identification of occult disease. In one study,
PET/CT revealed an occult site not detected by exam or standard imaging in 15% of patients. The
sensitivity of PET/CT in detecting active sarcoidosis is 80-90%. As specificity is low, tissue biopsy is
required to confirm the diagnosis. This case illustrates the utility of PET/CT in diagnosing extrathoracic
sarcoidosis. It is especially useful in those with unusual presentations and normal chest imaging.
177
INDIANA POSTER FINALIST - CLINICAL VIGNETTE Jinous Etemadi, MD
A Case of a 30 year old Presenting with a Rare Condition Disguised as B Cell
Lymphoma.
First Author: Jinous Etemadi, MD Co-Author: Ahmed Behery, MD
Langerhans cell histiocytosis (LHC) is a rare disease which more commonly affects children. It has a
widely variable clinical presentation that can mimic other conditions resulting in delayed diagnosis and
initiation of appropriate treatment. In this case a patient presented with recurrent B-symptoms that
were initially concerning for lymphoma.
A thirty year old African American male presented with six months duration of fatigue, night sweats,
polyarthralgia, and an unintentional twenty-five lb weight loss. In addition he also complained of
generalized bone pain and a diffuse scaly rash with extensive xerosis and peeling of skin over his trunk,
back, and extremities and had multiple previous episodes since 2004. On exam, non tender inguinal and
axillary lymphadenopathy was found. Given his presentation, lymphoma particularly B-cell was the
primary concern, followed by EBV and HIV. The patient was admitted and underwent an extensive work
up for the above conditions as well as for autoimmune and connective tissue diseases, which was
negative. Finally, an axillary lymph node excision biopsy revealed increased CD1a, and langerin positive
Langerhans cells as well as aggregates of histiocytes and eosinophils confirming the diagnosis of LCH.
The patient was then treated with a course of prednisone to which he responded with resolution of his
symptoms.
The exact pathogensis of LHC is unknown, however based on current hypotheses there is increased
proliferation of Langerhans cells with increased production of various cytokines, which contribute to the
constitutional symptoms seen in this case. The presentation of LHC is highly variable depending on the
extent of involvement which can range anywhere from benign single organ system to multifocal or
disseminated involvement with fatal consequences. In the majority of presentations reported there is
usually bone involvement and, to a much lesser extent, skin manifestations such as vesicular lesions as
well as dermatitis on the scalp or intertriginous regions. This case is unique in that the onset of
symptoms occurred during adulthood with an unusual skin findings and more pronounced constitutional
symptoms with lymphadenopathy which can be misleading for a lymphoma picture.
[Date]
This case exemplifies the importance of prompt consideration of rare diagnoses such as Langerhans cell
histiocytosis in patients presenting with B-symptoms and a negative work up for more common
conditions such as lymphoma or HIV in order to facilitate early treatment.
178
INDIANA POSTER FINALIST - CLINICAL VIGNETTE Rohan Mehta, MD
Salmonella isolation from perinephric abscess
First Author: Rohan Mehta, MD Second Author: Victor Collier, MD
Perinephric abscess can occur as a result of local spread, hematogenous or lymphatic seeding. The most
common etiologic organisms isolated include Staphylococcus aureus, Escherichia coli, and Proteus
species. Insidious presentation of the condition poses a significant challenge in diagnosis and the
subsequent appropriate medical or surgical intervention. The following is a very rare case in terms of the
organism isolate Salmonella sp. from a perinephric abscess.
A 44-year-old man with past medical history significant for End stage renal disease (ESRD) from
autosomal dominant polycystic kidney disease (ADPKD) presented to emergency department with a
fever of 102.9F and left lower quadrant abdominal pain. Two weeks prior to this visit, the patient had
intermittent fevers, vomiting, and non-bloody diarrhea for 5 days which resolved with supportive
treatment. Physical exam was positive for mild LLQ and flank pain without any urinary symptoms. CT
scan of the abdomen without contrast revealed bilateral renal enlargement and innumerable cysts
without any evidence of an infectious process. He was empirically treated with Vancomcyin and Zosyn.
However, he continued to have intermittent high grade fevers with severe leukocytosis and was
switched to intravenous ciprofloxacin concerning for possible cyst infection. A repeat CT showed some
left sided perinephric stranding confirming the suspicion of a cyst super infection but no definitive
abscess or fluid collection was visualized. He was transferred to our institution for further evaluation
and treatment, given his refractory fevers and leukocytosis. Antibiotics were switched to cefotaxime due
to improved cyst penetration and prior failure of ciprofloxacin. He remained febrile with significant LLQ
abdominal pain but repeat CT imaging showed a large abscess extending from the left kidney. He was
sent to interventional radiology for abscess drainage and cultures subsequently grew Salmonella sp.
Following drainage, he had resolution of fever and leukocytosis. He was discharged in stable condition to
complete two weeks of outpatient antibiotic therapy. Further review of outside records revealed that he
had grown a few Salmonella species from stool culture collected on admission.
[Date]
This case illustrates the difficulty in diagnosing perinephric abscess due to the slow onset of
presentation, radiographic limitations and the limited penetration of certain antibiotics. It also illustrates
that unusual pathogens can complicate the clinical picture. Although, most of the perinephric abscesses
are an extension of an intra-renal abscess rupture, up to 30 percent can present from a distant foci of
infection like gastrointestinal or pelvic structures through hematogenous or lymphatic spread It appears
this patient likely had salmonella enteritis followed by bacteremia, and possible hematogenous seeding
to his left kidney resulting in abscess formation. Recognition of this infection is essential to instituting
surgical drainage in concordance with appropriate penetrative antimicrobial therapy.
179
INDIANA POSTER FINALIST - CLINICAL VIGNETTE Wesley S Prichard, DO
Amiodarone-Induced Cirrhosis in the Absence of Long-Standing Transaminase
Elevation
First Author: Wesley S Prichard, DO, PGY-1, Department of Internal Medicine, St. Vincent's Hospital,
Indianapolis, IN. Second Authors: Laurel Fick, MD, Staff, Department of Internal Medicine, St. Vincent’s
Hospital, Indianapolis, IN. Jacob Richardville,
Amiodarone has been used for many years to treat various tachyarrhymias. While its side effect profile
includes hepatic toxicity, cirrhosis from amiodarone has been rarely reported.
A 74-year-old gentleman presented to the hospital with a progressive fifty-pound weight gain during the
previous three months despite increases in his home diuretic. He had no other complaints, and his
review of systems was otherwise negative. The patient denied a history of alcohol or illicit drug use. His
past medical history included coronary heart disease, systolic congestive heart failure, and atrial
fibrillation. His medications included amiodarone 200mg twice daily for 8 years, lasix, carvedilol,
atorvastatin, and aspirin. On exam the patient had anasarca including tense ascites and mildly elevated
jugular venous pressure and was otherwise normal and without evidence of stigmata of chronic liver
disease. A hepatic panel and coagulation studies were normal, including transaminases and alkaline
phosphatase, except for hypoalbuminemia of 1.8 mg/dL. Urinalysis revealed no proteinuria. A
transthoracic echocardiogram was unchanged from previous, showing an ejection fraction of 35%,
without signs of right-sided dysfunction and a high-normal right ventricular systolic pressure. A
computed tomography scan of the abdomen and pelvis revealed large-volume ascites and suggested
cirrhosis when compared to prior imaging. A review of his previous outpatient lab trends indicated
normal hepatic markers throughout the previous 10 years except for a brief period 6 months prior to
presentation with elevated transaminases to twice the upper limit of normal. Viral hepatitis serologies
were negative. An extensive laboratory workup, including ANA, AMA, Anti-Sm, ceruloplasmin, RF, antigliadin, alpha-1-antitrypsin, HIV, thyroid studies, iron studies, and HFE mutation was negative. A
paracentesis was performed which revealed normal cytology and cell counts and a SAAG of less than
1.1. The patient underwent a trans-jugular liver biopsy which revealed cirrhosis associated with bile
ductular proliferation and periductular neutrophilic inflammation and reported that drug-induced liver
injury should be considered. While the biopsy was atypical for amiodarone-induced cirrhosis, which
usually mirrors alcoholic liver disease with variable amounts of fibrosis, consultation with the
pathologist identified this medication as the most likely etiology for his cirrhosis.
[Date]
Asymptomatic transaminase elevation occurs in 25% of patients treated with amiodarone but only 1%
develop symptomatic acute or chronic liver dysfunction. A recent review article identified only 37 cases
of amiodarone-induced liver cirrhosis over a 42-year period. This rare case of amiodarone-induced liver
cirrhosis illustrates that hepatic injury can occur in the absence of chronically elevated hepatic
biomarkers. Clinicians should be aware that severe organ dysfunction can occur despite appropriate
monitoring and that amiodarone use should be avoided if possible to prevent this life-threatening
complication.
180
INDIANA POSTER FINALIST - CLINICAL VIGNETTE Harsh R Shah, DO
Unlucky 13: A Bleeding Mystery of an 88 year old female
First Author: Harsh R Shah, DO
Acquired Factor XIII deficiency due to anti-FXIII antibodies is a rare but life-threatening bleeding
disorder. Factor XIII is a fibrin stabilizing enzyme which crosslinks fibrin monomers. Deficiency of Factor
XIII results in destabilization of formed clots within 24-48 hours, resulting in delayed hemorrhage. Here,
we report a case of an 88-year-old female presenting with severe hemorrhage of unknown origin.
An 88-year-old female with a recent diagnosis of autoimmune hemolytic anemia on oral Prednisone
developed left arm swelling, pain, and ecchymosis. CT scan of the arm showed a biceps muscle
hematoma measuring 17cm in length. On the 4th day, she developed a rapidly evolving hematoma on
the contralateral forearm, which prompted bilateral fasciotomies and evacuation of multiple clots.
Patient had a normal coagulation profile and peripheral blood smear revealed features of chronic
hemolysis.
Subsequently, patient’s Factor XIII levels came back low at 8%. Testing for inhibitor with serial dilutions
showed an antibody titer of 1:40. Patient was started on 200mg of Cyclophosphamide and continued on
20mg of Prednisone for inhibitor eradication. On day 66, patient had AIHA flare up (Hg: 6.6g/dL) and was
started on Rituximab 375mg/m^2 weekly for 4 infusions. Her Factor XIII inhibitor level on day 68 came
up to 12% and inhibitor titer went down to 1:10. On day 98, patient developed several areas of large
ecchymosis on the right knee, thigh and buttock. Her Factor XIII activity dropped to < 10% again and
inhibitor titer went up to 1:20. She was transfused and was started on IVIG at 1000mg/kg X 5 days. Her
Factor XIII is still <10% but inhibitor titer is down to 1:10. Currently, patient is recovering in a rehab
institution and is not actively bleeding.
There are less than 60 reported cases of acquired factor XIII deficiency in the literature. In a systematic
review that looked at 28 cases, 79% of the patients presented with spontaneous hematomas and 18%
presented with ICH. 10 of the cases were associated with medications (5 with Isoniazid) and 7 with
autoimmune disorders. However, this is the first reported case presenting with warm antibody
hemolytic anemia. Mortality rate was 29% in general and 60% in patients presenting with ICH.
In conclusion, acquired FXIII deficiency is a rare bleeding disorder that can cause moderate to severe
bleeding and carries a significant mortality rate. This case illustrates the clinical paradigm that if a
patients presents with bleeding symptoms with no abnormal findings on routine tests, the possibility of
acquired FXIII deficiency should be considered. Prompt characterization of Factor XIII activity and
inhibitor level is essential in order to provide the most appropriate therapy for inhibitor eradication and
control of hemorrhagic complications.
[Date]
[1] Massimo et al. Acquired FXIII inhibitors: a systematic review. J Thromb Thrombolysis (2013) 36:109114.
181
IOWA POSTER FINALIST - CLINICAL VIGNETTE Snigdha Jain, MBBS
EBV Infection in an Immunocompromised Host: When “Mono” is Not Alone
First Author: Snigdha Jain, Resident Physician; Second author: Katherine Harris, Assistant Professor
A 20 year-old woman with a history of ulcerative colitis on azathioprine, primary sclerosing cholangitis
and hypothyroidism presented with high-grade fevers, malaise and mild right upper quadrant abdominal
pain unrelated to food intake. She presented to an outside emergency room one week prior to
admission with fevers and had been diagnosed with infectious mononucleosis. Physical examination was
significant for temperature of 38.5 C, tachycardia to 104 beats per minute, BP of 99/55 and mild right
upper quadrant tenderness with a negative Murphy’s sign. Laboratory testing revealed pancytopenia
with white blood cell count of 2.1, hemoglobin of 11.3 and platelets of 118, all of which were
significantly lower than her baseline levels while on azathioprine. Liver enzymes were mildly elevated in
a hepatocellular pattern. Abdominal ultrasound revealed splenomegaly without any evidence of
gallstones and a HIDA scan was negative for cholecystitis. Her immunosuppressive medications were
held and she was initially treated with supportive treatment of intravenous fluids. However, she
continued to have high fevers up to 40.5 C, tachycardia and worsening cytopenias. Concern for an
additional infectious etiology was raised and testing for atypical infections including Ehrlichia,
Anaplasma, Rickettsia, Crypotococcus, Leptospira and Cytomegalovirus was negative. She was started
on treatment with valacyclovir for EBV but continued to deteriorate clinically. As she was known to have
an autoimmune disease, Still’s disease, autoimmune hepatitis and vasculitides were also considered but
all specific immunologic testing was negative. Given her persistent fevers, cytopenias and splenomegaly,
concern for hemophagocytic lymphohistiocytosis (HLH) was raised. A ferritin level was checked and was
abnormally elevated to 7025 ng/ml, NK cell activity was found to be absent, soluble Interleukin-2
receptor activity was high and a bone marrow biopsy revealed hemophagocytosis, confirming the
diagnosis of HLH. She was treated with intravenous immunoglobulin, dexamethasone, anakinra and
cyclosporine. Her fevers and fatigue resolved and her laboratory values returned to normal within a few
weeks of treatment.
[Date]
Hemophagocytic lymphohistiocytosis (HLH) is a syndrome characterized by systemic immune activation
leading to massive inflammation and cytokine release. It is known to be under- diagnosed given its nonspecific clinical manifestations that may overlap with any infectious or inflammatory process. It is a rare
but life – threatening disorder that requires a high index of suspicion for diagnosis. This case illustrates
that clinical signs and symptoms out of proportion to that expected from a common infection should
prompt consideration of an additional systemic inflammatory process, even in an immunocompromised
patient, as appropriate and timely treatment can be life saving.
182
IOWA POSTER FINALIST - CLINICAL VIGNETTE Megan L Srinivas, MD
Mycophenolate-Induced Disseminated TB in a PPD-Negative Patient
Megan L. Srinivas, PGY-1, Bayview Internal Medicine, Johns Hopkins University, Baltimore, Maryland
Individuals with underlying rheumatologic diseases such as dermatomyositis may not adequately
respond to tuberculin (PPD) skin tests, creating false negative results. These illnesses are frequently
treated with immunosuppressive therapy making proper identification of TB infection imperative.
A 59-year-old Filipino man was diagnosed with dermatomyositis on the basis of rash, electromyography,
and muscle biopsy. He was initially treated with IVIG infusions and transitioned to oral prednisone and
mycophenolate. The patient’s symptoms improved on this regimen. Six months after starting
mycophenolate, the patient began having fevers, night sweats, and productive cough without
hemoptysis. He moved from the Philippines 5 years prior to dermatomyositis diagnosis, denied sick
contacts, and was PPD negative both at immigration and immediately prior to starting mycophenolate
treatment. A third PPD was negative following the onset of these new symptoms. He was treated for
community-acquired pneumonia, but symptoms worsened over 10 days and he developed watery
diarrhea and a growing non-tender, non-mobile mass on the left side of his neck. A chest x-ray
demonstrated a cavitary lesion in right upper lobe suspicious for TB that hadn’t been present one month
earlier. Chest CT corroborated this finding also exhibiting necrotic hilar and paratracheal
lymphadenopathy. Neck CT demonstrated the left-sided mass as cervical chain
lymphadenopathy. Expectorated sputum and stool samples contained acid-fast bacilli (AFB), cultures
showing TB bacteria. Fine-needle biopsy of the neck mass (scrofula) also exhibited AFB. An MRI brain
showed nodular enhancement suspected to be a tuberculoma. Mycophenolate was discontinued and
dermatomyositis treatment was switched to oral prednisone with a 3-day course of IVIG. The patient’s
infection showed sensitivity to standard RIPE (rifampin, isoniazid, pyrazinamide, and ethambutol)
treatment. Within a week of starting RIPE, the patient’s diarrhea subsided, scrofula diminished, and
symptoms significantly improved. By the end of treatment week 3, the patient’s sputum no longer
contained AFB; he was removed from isolation, and was discharged to continue RIPE at home. He was
discharged on oral prednisone, which effectively addressed his dermatomyositis.
[Date]
This case illustrates the unreliability of PPD tests in patients with long-term inflammatory diseases such
as dermatomyositis. Other immunosuppressive therapies (adalimumab, etanercept, and infliximab)
have been affiliated with conversion of latent TB to disseminated TB. Mycophenolate is another
immunosuppressive agent with similar mechanistic properties. Thus, it is imperative that patients with
long-term inflammatory diseases and high-risk TB factors initiating immunosuppressive therapy receive
a TB blood test (such as a quantiferon gold assay) prior to the initiation of therapy to ensure that latent
TB is unmasked before it can evolve into a disseminated form of the disease.
183
IOWA POSTER FINALIST - CLINICAL VIGNETTE Maria T Story, MD
All That Glitters is not Gold
First Author: Maria T Story, MD, Second Author: Sarat Kuppachi, MD
A 63 yo healthy male, with no past medical history or allergies, presented to the Emergency Department with
a rash and facial swelling of four days duration. He had been receiving intravenous Vancomycin and
Ceftriaxone for 18 days after a transesophageal echocardiogram (TEE), performed to evaluate recurrent
fevers, demonstrated ‘a small mobile mass on the non-coronary cusp of the aortic valve, possibly a
'vegetation.' Six blood cultures prior to TEE were negative.
On admission vital signs included BP 119/67, HR 101, and T39.6 C. Skin examination showed periorbital and
facial edema and erythematous patches overlying diffuse edema of the entire body. There were no oral
ulcerations or lymphadenopathy. Palms and soles had slightly purpuric macules present. There was no
murmur on auscultation. Laboratory studies were notable for 22,000 WBCs, predominantly neutrophils and
bands, and 1358 eosinophils. LFTs were not elevated.
To exclude the possibility of infective endocarditis, a repeat TEE was performed. The new study
demonstrated ‘echodensities at the edges of both the non-coronary and left coronary cusps of the aortic
valve, likely benign hypertrophied Nodules of Arantius.’ When compared with previous images, the findings
had not changed.
Despite discontinuing antibiotics the rash evolved into body-wide erythroderma, which led to diffuse
desquamation and formation of pseudovesicles on the arms and trunk. Skin biopsy demonstrated a
perivascular lymphoid infiltrate consistent with an atypical lymphomatoid drug eruption.
Drug Reaction with Eosinophila and Systemic Symptoms (DRESS) syndrome, resulting from unnecessary
antibiotic usage for a benign echocardiographic finding, led to significant morbidity. Clinicians should
recognize features of infective vegetation’s to be confident in the diagnosis of infective endocarditis before
committing patients to prolonged courses of antibiotics. The key features of infective vegetation’s include a
pedunculated mobile echodensity, typically on the free margin of the leaflet. Aortic vegetation’s are normally
present on the ventricular surface of the valve and leaflet thickening is absent.
Our patient recovered well on a prolonged steroid taper.
[Date]
The difficult search for the source of fever should not excuse the exclusion of scientific rigor that is firmly
evidence based. In this case we are unable to determine the indication for the TEE in the absence of a
detectable murmur. Critical evaluation of the entire clinical picture, including absence of new heart murmur,
multiple negative blood cultures, lack of physical findings suggestive of endocarditis, and atypical findings of a
‘mass’ on echocardiogram could have prevented these life threatening complications. Evidence shows that
adults who remain undiagnosed after an extensive evaluation for fever of unknown origin have a good
prognosis. Approaching treatment strategies because 'we have to do something' is not good practice. This
case highlights potential life threatening dangers in deciding that ‘this should work’ especially in the absence
of clinical evidence. All that glitters isn’t gold, similarly all vegetation’s found on cardiac valves are not
infectious…even if the patient is febrile.
184
IOWA POSTER FINALIST - CLINICAL VIGNETTE Alexis I Wickersham, MD
Postpartum Chest Pain and Cardiac Arrest
Alexis Wickersham, MD
Mrs. AM is a 31 y.o. G3P3 female with a witnessed cardiac arrest due to ventricular fibrillation (VF). She
was 6 weeks postpartum following an uncomplicated pregnancy and delivery were uncomplicated. She
had presented to the emergency department (ED) of a local hospital with severe retrosternal chest pain
and shortness of breath that started earlier that day. In the ED, she became unresponsive and was found
to be in VF. Cardiopulmonary resuscitation was started immediately. After return of pulse, a12-lead EKG
showed ST-elevation in anterolateral leads. Coronary angiography showed diffuse spasm in the mid left
anterior descending (LAD) artery with good distal flow. Left ventriculography showed apical dyskinesis
and ballooning with hyperdynamic basal segments. Estimated ejection fraction (EF) was 15%. She was
transferred to our hospital with a diagnosis of stress-induced cardiomyopathy. Upon arrival, she was
chest pain free with borderline low blood pressure. Bedside Swan-Ganz catheter showed low cardiac
index, elevated filling pressures and high SVR consistent with cardiogenic shock. She was started on
nitroprusside for afterload reduction. Laboratory studies were significant for an elevation in troponin-T
(5.09 ng/mL) and CK (3553 U/L). C-reactive protein, D-dimer and respiratory viral PCR were negative.
Cardiac MRI showed severely depressed left ventricle (LV) systolic function and extensive transmural
scar in anterior wall with matched wall motion abnormality suggesting a diagnosis of myocardial
infarction. Coronary CT angiography was performed that showed a dissection flap with a false lumen in
the LAD. Given the CT and MRI findings, a diagnosis of spontaneous dissection of LAD leading to acute
myocardial infarction was made.
[Date]
Spontaneous coronary artery dissection is rare, but should be considered as possible etiology of an
acute myocardial infarction (MI) in a young patient, especially women in the peri-partum period.
Increased hemodynamic stress or arterial wall changes from hormonal effects during pregnancy have
been proposed as potential mechanisms. Patients typically present with chest pain, EKG findings
consistent with ST-elevation MI and/or cardiac arrest. The diagnosis is commonly made during coronary
angiography or other cardiac imaging modalities. Treatment should be based on symptoms, clinical
status and affected coronary segments. Although, immediate revascularization may limit myocardial
damage, percutaneous coronary intervention can be challenging due to potential for propagation of the
dissection flap. Bypass surgery may be considered in unstable patients and in dissections involving the
left main artery. Conservative treatment is preferred in stable patients and with dissections involving
small arteries.
185
KANSAS POSTER FINALIST - CLINICAL VIGNETTE Anjalee Goel Carlson, DO
Testicular Sarcoidosis
First Author: Anjalee Goel Carlson, DO Second Author: Timothy Shaver, MD
Testicular germ cell tumors (GCT) are the most common solid tumors in young men. However, there
have only been a few cases of patients with sarcoidosis or sarcoid-like reaction with testicular GCT.
Sarcoidosis is an idiopathic, multisystem disease involving the development of non-caseating
granulomas, primarily in the lung. There is a 1.1% cumulative incidence of sarcoidosis occurrence with or
following testicular cancer. Furthermore, the distinction between sarcoidosis and testicular GCT with
metastasis can be difficult as pulmonary hilar lymphadenopathy is present in 90% of genitourinary
sarcoidosis cases. Therefore, genitourinary sarcoidosis may mimic a testicular GCT in males as both
occur in the same age group of males. In patients that present with sarcoidosis symptoms and a
testicular mass, sarcoidosis or sarcoid-like granulomatosis with testicular GCT should be considered in
the differential diagnosis. It is important to note that the treatment of GCT has drastically changed and
has more than 80% curative rate with current chemotherapy regimens.
A 29-year-old African American male presented with symptoms of cutaneous lesions, lymphadenopathy,
and unilateral painless swelling of his left testicle. Lymph node biopsy was performed displaying
noncaseating granulomas consistent with diffuse disseminated sarcoidosis. Testicular biopsy also was
performed due to the increased risk of sarcoid-like granulomatosis with testicular germ cell tumors.
Frozen section was consistent with sarcoid granulomatosis. Steroid therapy was initiated and marked
improvement was noticed by time of discharge.
[Date]
Although this patient did not have a testicular GCT, it is essential that the patient be managed as if it is
high on the differential as the outcome is based primarily on the initiation of treatment. Since both
genitourinary sarcoidosis and testicular GCT present in patients of the same age and clinically may
present the same, it is essential to keep both in consideration. Patients with sarcoid-like symptoms and
testicular enlargement or mass need to be evaluated for testicular cancer, as there is an elevated risk for
coexistence of sarcoid-like granulomatosis and testicular GCT.
186
KANSAS POSTER FINALIST - CLINICAL VIGNETTE Kaitlin M Ditch, MD
STORM IN AN UNSUSPECTING PATIENT
First Author: Kaitlin M Ditch, MD Georges Elhomsy, M.D.
Introduction: Thyroid storm is an extreme accentuation of thyrotoxicosis that occurs primarily in patients
with untreated Graves’ disease but can occur in patients with toxic multinodular goiter. It is usually
precipitated by surgery, trauma or infection. It is characterized by symptoms of severe hypermetabolism.
Fever is almost always existent. Tachycardia and arrhythmias may be associated with heart failure. Delirium
and psychosis may occur and progress to stupor and coma (1). Although rare (2), thyroid storm has a
mortality rate of 20 to 50% (1).
Case Description: A 28 year old female with medical history of asthma presented to the emergency
department with three week history of upper respiratory symptoms and chest pain. The physical exam
revealed temperature of 100.2°F, pulse of 159 bmp and bilateral wheezing, decreased air entry and increased
expiratory phase. EKG revealed supraventricular tachycardia that did not respond to several doses of
adenosine. Cardizem drip was initiated and synchronized cardioversion was performed but without success.
Later she developed respiratory failure and was intubated. Laboratory evaluation revealed leukocytosis, lactic
acidosis, and normal urinalysis. Imaging showed no abnormalities. She was treated for asthma exacerbation
and community acquired pneumonia. Later, sputum culture was positive for Oxacillin sensitive
staphylococcus aureus, and nasopharyngeal swab was positive for coronavirus.
On the fourth day of admission the patient was successfully extubated; however, she was still stuporous,
tachycardic febrile and had elevated LFTs. Only then were her thyroid function tests ordered and revealed
low TSH 0.08 uIU/mL (0.35-5.50 mIU/mL), elevated total T3 332 ng/dL (87-178 ng/dL), elevated free T4 5.2
ng/dL (0.6-1.1 ng/dL), and elevated Thyroid Stimulating Immunoglobulin. The patient was diagnosed with
thyroid storm with Wartofsky score of 80, highly suggestive of thyroid storm. She was treated with
methimazole, propranolol, hydrocortisone, and SSKI. Shortly after, the patient improved dramatically, with
resolution of her fever, tachycardia and neurological symptoms. She was discharged home one week later.
Discussion/Conclusion: The Burch-Wartofsky Scores (1) is a clinical tool that can help confirm the diagnosis of
thyroid storm. Score of 45 or greater indicate thyroid storm while scores less than 25 are unlikely thyroid
storm. The score’s parameters are temperature, CNS effects, cardiovascular dysfunction (Tachycardia, A-Fib,
CHF) gastrointestinal-hepatic dysfunction and precipitant events, Thyroid storm should be treated with
thionamide (Methimazole or PTU) to block thyroid hormone production, Potassium iodide (SSKI) to prevent
thyroid hormone release and should be given at least one hour after thionamide, hydrocortisone to decrease
peripheral conversion of T4 to T3 and propranolol to control heart rate.
While thyroid storm is rare, its high mortality suggests that it should be considered in the differential
diagnosis of the critically ill patient with hyperpyrexia and tachycardia. Thus, we recommend checking thyroid
function tests in these patients.
Akamizu T., Satoh T., Isozaki O., et al. Diagnostic criteria, clinical features, and incidence of thyroid storm based on nationwide surgerys. Thyroid
2012; 22:661. (2)
[Date]
References: Burch H.B., Wartofsky L. Life-threatening thyrotoxicosis. Thyroid storm. Endocrinol Metab Clin North Am 1993; 22:263. (1)
187
KANSAS POSTER FINALIST - CLINICAL VIGNETTE Justin G Fernandez, MD
Undiagnosed Systemic Lupus Erythematous Presenting as Hemophagocytic
Lymphohistiocytosis
First Author: Justin G Fernandez, MD Christopher Dakhil, M.D.
Hemophagocytic lymphohistiocytosis (HLH) is a rare disease that occurs primarily in the pediatric
population. When diagnosed in adults, it is usually known as secondary HLH. Incidence is reported as
roughly one case per million persons per year. It can be triggered by conditions that affect immune
homeostasis such as infections, genetic mutations and rheumatologic disorders. The following case
demonstrates a rare instance in which undiagnosed systemic lupus erythematosus (SLE) resulted in
HLH.
A 28 year-old male with no past medical history and a recent unremarkable cervical lymph node biopsy
presented with progressive weakness, flu-like symptoms and recurrent fever of 2 months. Vital signs
were within normal limits except for temperature, which was 100.30F. His exam was unremarkable
except for a malar rash and a left cervical scar from the aforementioned lymph node biopsy. His labs
showed pancytopenia, neutropenia, positive antinuclear antibody, hypertriglyceridemia, fibrinogen of
126 mg/dl, ferritin >40,000 ng/ml and hemophagocytosis was present on bone marrow biopsy. All
workup for a source of infection was negative. A tentative diagnosis of HLH was made based on clinical
presentation and the above laboratory data, which satisfied the HLH-2004 trial diagnostic criteria. The
patient was then transferred to a regional quaternary medical center and was treated with an HLH
protocol using etoposide and dexamethasone. Later, it was determined that the disease was secondary
HLH after a workup of his malar rash revealed SLE. The patient was treated for SLE with an
immunosuppressive regimen of cyclosporine and dexamethasone, and he improved dramatically. He
was eventually discharged home in stable condition.
[Date]
Adult HLH usually presents secondary to infection but is rarely due to a rheumatologic condition such as
SLE. Diagnosis may be difficult as there is frequently an overlap in the clinical and laboratory picture.
This diagnosis should always be kept in mind when those with rheumatologic conditions acutely
decompensate and present with multiple blood abnormalities.
188
KANSAS POSTER FINALIST - CLINICAL VIGNETTE Rossa Khalaf, MD
Multiple Myeloma as Cyclic Vomiting Syndrome
First Author: ROSSA KHALAF, Nassim Nabbout, MD, FACP
Introduction: Multiple myeloma (MM) is a neoplastic proliferation of immunoglobulin-producing plasma
cells that accounts for 10% of hematological malignancies and 1% of all cancers in the USA. It mainly
presents with hypercalcemia, renal failure, anemia of chronic disease, and lytic bone lesions with bone
pain. Rarely, patients may have neurologic disorders present involving the central and peripheral
nervous systems. With this clinical picture, diagnosis is established with presence of protein M >3 g/dl in
serum/and urine and presence of 10% or more clonal plasma cells. We present a patient who presented
with cyclic vomiting syndrome (CVS) for a year before the diagnosis of MM was made.
Case report: A 58-year-old female with a past medical history of chronic normocytic anemia and
hypertension presented with recurrent nausea, bilious vomiting, and intermittent constipation over a
period of fourteen months. These presentations were associated with dehydration and acute kidney
injury that would resolve with hydration. Workup, including EGD, colonoscopy, CT of the
abdomen/pelvic, MRI of the brain, UDS, and gastric emptying, was negative. A diagnosis of cyclic nausea
and vomiting disorder was made. Over the ensuing 14 months with continued symptoms, unintentional
weight loss, emergency room visits, and repeat imaging, there was an incidental finding of diffuse pelvic
bone and spine lytic lesions on CT scan. During this period, creatinine and, calcium were normal;
hemoglobin was within the patient’s baseline with usual normocytic normochromic anemia. Further
workup revealed +2 rouleaux formation, M-Spike elevation, and Kappa/lambda ratio of 43.9. Bone
marrow biopsy showed 90% cellularity of which 80% were plasma cells. A diagnosis of diffuse pattern of
multiple myeloma was confirmed and patient was started on chemotherapy regimen of bortezomib.
[Date]
Conclusion: This patient’s cyclical vomiting presentation is explained by multiple myeloma induced
neuropathy. This process is explained by diverse etiologies including compressive, plasma cell infiltrative
or autoimmune/cytokines mediated. Diagnosis of multiple myeloma can be challenging and requires a
high index of suspicion to establish the diagnosis early since this affects prognosis. Clinicians should have
a judicious clinical approach to detect multiple myeloma especially when the classical presenting
symptoms of CRAB (elevated Calcium, Renal failure, Anemia, Bone lesions) are absent.
189
KENTUCKY POSTER FINALIST - CLINICAL VIGNETTE Michael E Jesinger, MD
TRIPOLAR DISORDER
Michael Jesinger,MD Archana Narla,MD Romil Chadha,MD
Learning Objectives:
·
Describe a rare presentation of acute on chronic lithium toxicity
·
Highlight complications of lithium therapy and outline treatment options
Case Presentation: A 55 year-old lady with history of bipolar disorder presented with worsening of
mood and visual hallucinations for two weeks. Her bipolar disorder was well-controlled with lithium
over the last 20 years; she recently increased her lithium dose in order to control her symptoms better.
Her exam was notable for bradycardia, fine intention tremors, apraxia, confusion and slurred speech.
Laboratory workup revealed acute kidney injury with creatinine of 2.5 mg/dl and elevated lithium level
of 3.6 mmol/L. Lithium was discontinued and fluid resuscitation was initiated. However, she became
obtunded and repeat lab work revealed severe hypernatremia (164mmol/l), hypercalcemia (iCa
5.8mmol/l) and elevated parathyroid hormone (422pg/ml) consistent with lithium induced nephrogenic
diabetes insipidus and lithium induced primary hyperparathyroidism. She was started on free water and
amiloride to take care of nephrogenic diabetes insipidus. Even with one slow hemodialysis session the
lithium level normalized with full recovery of her mental status. Initiation of cinacalcet corrected her
calcium. By time of discharge she regained her full functionality and sensorium.
[Date]
Discussion: Lithium is an effective and widely used medication for mood. However, lithium has a narrow
therapeutic index with frequent toxicity during treatment. Acute lithium poisoning typically presents
with nausea, vomiting and diarrhea; with neurologic findings such as confusion, agitation and ataxia
developing late. A common but often unrecognized complication of long-term lithium therapy is
hyperparathyroidism and associated hypercalcemia and hypocalciuria. The exact mechanism by which
lithium increases serum calcium levels is unknown but may be due to an increased threshold for the
calcium-sensing mechanism within the parathyroid gland, overproduction of PTH by inhibiting the action
of GSK 3b, and inhibition of calcium transport across cell membranes. Renal failure often complicates
hypercalcemia which leads to concurrent hypocalciuria. Approximately 10% of patients taking Lithium
will develop hypercalcemia, and hypocalciuria with a smaller percentage having a high serum PTH
concentration. Compared to the general population affected by hyperparathyroidism, higher percentage
of patients (33%) develop parathyroid hyperplasia in lithium-induced hyperparathyroidism. This
hyperplasia is the probable reason why acute discontinuation of lithium does not result in immediate
changes in calcium homeostasis. Treatment is with discontinuation of lithium. If hypercalemia does not
resolve after discontinuation, parathyroidectomy may be an alternative in select populations. In
addition, there have been case reports describing the use of cinacalcet; a calcimimetic drug that may be
used to decrease or normalize the serum calcium. This may be a good option for non-surgical candidates
currently and in future has potential to become the drug of choice for lithium induced primary
hyperparathyroidism.
190
KENTUCKY POSTER FINALIST - CLINICAL VIGNETTE Justin R Kingery, MD PhD
“You’re Not Dying” and Other Acceptable Lies: Ethical Communication in Global
Health
Justin R Kingery, MD/PhD, Francesca P Kingery MS3 1Department of Medicine 2University of Louisville
School of Medicine
The concept of “global health” is ever evolving and becoming a core of medical education. As western
trained physicians transition to practicing medicine in the developed world, due to limited resources,
they are presented with the challenge of making decisions based less on diagnostic tools and rely more
on clinical judgment. The ethical principles of autonomy, beneficence, non-maleficence and justice are
also a core of western medical education.
[Date]
This case describes a 45 yo Kenyan patient with stage IV esophageal cancer examined by a U.S. medical
team and determined to be appropriate for end of life care. Upon informing the family of their options,
a translator intervened noting that it is “unacceptable” to provide negative information regarding death
and possible poor outcomes and that “discouragement” of the patient and family would be detrimental
to the patient’s health. The medical team was ultimately faced with the ethical decision of 1) adhere to
local norms and “encourage the patient” at risk of negative association of death with visiting physicians
vs 2) adhere to western medical values of patient autonomy and justice by describing the likely
outcome. This case further explores the concept of “truth-telling” in healthcare and ultimately,
questions if western principles of ethics apply in the global health setting. An argument for respecting
the Kenyan culture hinges on the concept that they are comprised mostly of a collectivist society,
therefore, patient autonomy is less of a factor. Individualist societies, such as the United States, value
patient autonomy over “encouragement” of the family structure. Ultimately, culturally sensitive
research methods to explore these differences and preferences are both valuable and needed.
191
LOUISIANA POSTER FINALIST - CLINICAL VIGNETTE Ramsy A Abdelghani, MD
Early Continuous Venovenous Hemodiafiltration in Preventing Permanent Kidney
Injury in Severe Rhabdomyolysis
First Author: Ramsy A Abdelghani, MD Senior Author: Jones Samuel, MD
Acute kidney injury (AKI) associated with increased pigment load in rhabdomyolysis can often lead to
irreversible kidney damage. Traditional means of pigment removal are often insufficient. Recent trends
have shown the use of continuous venovenous hemodiafiltration (CVVHDF) using a high-flux dialyzer in
severe cases of rhabdomyolysis can lessen these irreversible effects. However, the optimal timing of
CVVHDF initiation, as well as its efficacy, is still controversial. We present a case of severe
rhabdomyolysis admitted to our ICU where early CVVHDF decreased irreversible kidney injury in the
patient.
A previously healthy 37 year old African American female with no significant past medical presented to
our hospital complaining of bilateral lower extremity pain that began earlier that day. On examination,
the patient had weak, cool lower extremities. In addition, the patient had no sensation and no palpable
pulses in her lower extremities. The patient was found to have acute bilateral common femoral
thromoemboli, which required fasciotomy and ultimately, a right above the knee amputation (AKA). On
labs, the patient had an anion gap metabolic acidosis with anion gap of 24. Serum Creatinine Kinase
(CPK) and myoglobin were 2,331,300 U/L and 152,414 ng/mL, respectively. Pt had oliguria of <
0.5ml/kg.hr with a peak serum creatinine of 1.8 mg/dL (GFR 41 mL/min/1.73). Due to the high pigment
load and lack of response to volume resuscitation, the patient was dialyzed with immediate CVVHDF in
an attempt to preserve kidney function. The patient was weaned off dialysis, and at discharge, the
patient’s creatinine was 1.4 mg/dL (GFR of 54 mL/min/1.73).
[Date]
Our case adds to the theory that early CVVHDF can help preserve vital kidney function over traditional
dialysis due to its ability to clear myoglobin more effectively. Therefore, we believe CVVHDF should be
considered in patients with AKI secondary to severe rhabdomyolysis. Further larger studies are needed
to determine additional benefits, common complications, and contraindications to CVVHDF in AKI
secondary to severe rhabdomyolysis.
192
LOUISIANA POSTER FINALIST - CLINICAL VIGNETTE John B Rhodes Jr, MD
Arterial Fistulization to the Duodenum as a Complication of Chronic Pancreatitis: A
Case Report
First Author: J. Brent Rhodes, Jr. Second Author: Angela Johnson
Introduction: Chronic pancreatitis is associated with serious potential complications. Most commonly,
this is secondary to pseudoaneurysm formation or direct complication of surgical intervention. Here, we
discuss the case of a 39 year old man with chronic pancreatitis complicated by arterial fistulization of the
duodenum.
Case: A 39 year old male with past medical history of hypertension and alcohol abuse presented with
severe abdominal pain, localized to the epigastrum and right upper quadrant. This led to multiple
emergency department visits, culminating in a diagnosis of gallstone pancreatitis. The patient
underwent elective laparoscopic cholecystectomy, but returned five days later with continued
abdominal pain, elevated lipase, and transaminitis. ERCP was unsuccessful secondary to duodenal wall
edema. Repeat imaging demonstrated a complex process in the region of the pancreatic head
consistent with a large hematoma versus pseudocyst with concern for compressive physiology. An
external biliary drain was placed and the patient improved somewhat over the next several days. On
hospital day 15, he was noted to have multiple large, bloody bowel movements. Emergent
esophagogastroduodenoscopy was performed demonstrating fresh blood in the duodenum, but no
identifiable source for intervention. He was subsequently transferred to the ICU. Emergent arteriogram
was performed, revealing active hemorrhage from a proximal branch of the superior mesenteric artery,
thought to be the inferior pancreaticoduodenal artery, which was then embolized. The patient had
several more episodes of large bloody bowel movements associated with hemodynamic instability, and
required two futher coil embolizations. Due to the patient's high surgical risk, operative intervention
was deferred. After several more episodes of acute hemorrhage and over sixty units of packed red
blood cells transfused during his stay, the patient was taken to the operating room on hospital day 45,
where intraoperatively, a fistula between the inferior pancreaticoduodenal artery and the second
portion of the duodenum was identified and repaired. The patient was stable postoperatively and was
transferred to the floor four days later. He had no further episodes of acute bleeding and was
discharged to home in stable condition.
[Date]
Discussion: This case illustrates the potential for life threatening vascular complications of chronic
pancreatitis. Classically, acute blood loss results from rupture of pseudoaneurysms, as a result of
surgical intervention, or as indirect upper gastrointestinal bleeds from peptic ulcers or esophageal
varices. In this case, we present the direct fistulization of the duodenum from the inferior
pancreaticoduodenal artery, which from our literature search is a previously undescribed entity. This
significant finding must be considered as an etiology in future cases of acute gastrointestinal blood loss
following pancreatitis.
193
LOUISIANA POSTER FINALIST - CLINICAL VIGNETTE Jonathan R Schroeder, MD
Massive Pulmonary Embolism: A rare presentation of Acute HIV-1 Infection
First Author: Jonathan R Schroeder, MD Second Author: William Varnado, MD Third Author: Catherine
O'neal, MD Fourth Author: Vince Cataldo, MD
INTRODUCTION: Acute HIV infection rarely presents as venous thromboembolism with only 6 described
cases in the medical literature. HIV infection predisposes to hypercoagulability by a number of
pathways.
DESCRIPTION: An 18 year old male with scalp psoriasis (initiated on adalimumab two weeks prior)
presented to the emergency department complaining of dyspnea on exertion, pleuritic chest pain, and
left leg pain for 2 weeks. Review of systems also revealed one month of subjective fevers, malaise, and
headaches. His vital signs revealed mild hypoxemia and tachycardia. An activated partial thromboplastin
time (aPTT) was prolonged at 58 seconds and his platelets were decreased at 100,000 / ul. Lower
extremity compressive venous ultrasonography revealed acute deep venous thrombosis (DVT) of the left
popliteal vein and computed-tomography (CT) angiogram of the chest revealed extensive bilateral
pulmonary emboli and a large saddle embolus, pulmonary infarction, and hepatosplenomegaly.
Selective pulmonary angiography with targeted thrombolysis confirmed bilateral pulmonary artery
emboli. His hospitalization was complicated by progressive severe thrombocytopenia and fevers with
rigors. His social history revealed he had experienced his first unprotected sexual encounter with a man
one month prior to symptoms. HIV antibodies were positive and a quantitative viral load revealed 4
million copies per ml and a CD4+ lymphocyte count was recorded at 534 cells per ml. Assays for anticardiolipin antibodies and ß-2-glycoprotein antibodies were positive. He received empiric treatment for
the anti-phospholipid syndrome and heparin-induced thrombotic thrombocytopenia, dose-adjusted
bivalirudin was substituted for heparin as a bridge to warfarin. Anti-retroviral therapy and intravenous
immunoglobulin were also initiated for HIV-associated thrombocytopenia. His platelets improved and
were stable on discharge. The patient was asymptomatic and compliant with ART and warfarin therapy
at a four week follow up appointment and laboratory revealed normal complete blood counts and a
marked reduction in viral load with only 119 copies / ml detected.
[Date]
DISCUSSION: HIV infection has been associated with syndromes of thrombosis and thrombocytopenia
including acquired coagulation factor abnormalities, the presence of anti-phospholipid antibodies,
heparin-induced thrombocytopenia, and thrombotic thrombocytopenic purpura-hemolytic uremic
syndrome. These syndromes are more commonly associated with advanced HIV infection and AIDS,
however thrombosis and thrombocytopenia are a rare complication of early HIV infection likely as a
result of intense viremia and inflammation leading to endothelial dysfunction. HIV screening status
should be considered at all patient encounters. The initiation of anti-TNF therapy, which has been
associated with thrombosis, or unexplained thromboembolism should also prompt consideration of
screening for HIV.
194
MAINE POSTER FINALIST - CLINICAL VIGNETTE David J Buzanoski, MD
An Unusual Complication of Crohn’s Disease: Neuro-Enteric Fistula and Gram
Negative Rod Meningitis
David J Buzanoski, MD
Introduction: Fistula formation remains a significant issue for patients with Crohn’s Disease. Although most fistulas
are either perianal or entero-enteric, the tracts may involve many sites. Posteriorly fistulizing disease is an
uncommon complication of Crohn’s Disease that poses a diagnostic challenge due to a lack of associated
gastrointestinal symptoms. This case describes an individual with extensive infectious complications, including a
neuro-enteric fistula and meningitis, resulting from fistulizing Crohn’s Disease.
Case Presentation: A 31 year old male with a history of Crohn’s Disease was transferred to our hospital for
workup and treatment of meningitis. Symptoms of fever, headache, and back pain had been present for 1 week.
He had also suffered from months of progressive back pain and leg weakness. Since his diagnosis of Crohn’s 15
months prior, the patient had been unable to wean from steroids and remained on prednisone & azathioprine. In
the weeks preceding admission, he experienced no worsening abdominal symptoms.
Physical exam revealed a cachectic male with normal vital signs, nuchal rigidity, and photophobia. Abdominal exam
revealed right sided tenderness, and his right leg was held in full flexion. Extending the leg was painful. There were
no focal neurologic deficits.
CBC demonstrated WBC: 18.1, hemoglobin: 9.3 mg/dL, and platelets: 278,000. Blood cultures from the outside
hospital grew Bacteroides fragilis and Aggregatibacter segnis. CSF, also obtained prior to transfer, showed WBC:
445 and protein > 600 mg/dL. CSF culture was also polymicrobial, with Escherichia coli and A. segnis isolated.
CT of the abdomen/pelvis demonstrated severe inflammation, strictures of the distal ileum & sigmoid colon,
several psoas abscesses, and multiple fistulous tracts - including neuro-enteric fistulas associated with air-fluid
collections throughout the presacral space, sacrum, epidural space, and psoas muscles. MRI showed L5-S1 diskitis,
an epidural abscess (L4 to S1), and sacral osteomyelitis.
The patient responded to antibiotic therapy and did not require neurosurgical intervention for the epidural
abscess. Psoas abscesses were drained by interventional radiology. Bowel resection and diverting ileostomy were
performed during the hospitalization. He required weeks of parenteral nutrition before tolerating oral intake. His
functional status improved throughout the hospitalization, and he ambulated without assistance by the time of
discharge.
Although rare, multiple case reports describe neuro-enteric fistulas causing epidural abscess or meningitis. The risk
of such occurrences highlights the importance of maintaining a high index of suspicion when evaluating a Crohn’s
Disease patient with new or progressive back pain. Such patients may warrant earlier consideration for diagnostic
imaging targeting both spinal and intra-abdominal pathology.
[Date]
Discussion: Fistula formation is a common complication of Crohn’s Disease, with some studies estimating an
incidence of nearly 35% in the 10 years following diagnosis. Only a small percentage of fistulas extend to
retroperitoneal structures, with the most common complication being psoas abscess formation. These
complications pose a diagnostic challenge due to the frequent absence of typical abdominal symptoms.
195
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Selwan Bangean Abdullah, MD
Ependymoma: Surprising Explanation of Neurologic Findings in an untreated SLE
patient
First Author: Selwan Bangean Abdullah, MD 2nd Author: Sarah Finn, MD 3rd Author: Rudolf Pullmann
Introduction: Patients with systemic lupus erythematosus (SLE) may present with various neurological
manifestations including stroke, cognitive dysfunction, seizure, headache, psychiatric disorders or
neuropathies. In this case, we present a patient with progressive memory loss, right sided weakness and
central facial nerve palsy originally attributed to SLE, but later found to be due to ependymoma
involving brainstem.
Case: 28 year old woman with a history of SLE and antiphospholipid syndrome presented with right
facial and arm weakness and numbness, headaches, and memory loss. She was on plaquenil, but
discontinued it for 6 weeks after losing her insurance. Prior to presentation, she experienced symptoms
of a typical flair including fevers, fatigue, aphtous ulcers, and joint pain. She was nauseated and noticed
she could not taste anything on the anterior aspect of the right side of tongue. Later she developed a
right facial droop which progressed to right arm and leg weakness. She was diagnosed with Bell's palsy
and prescribed prednisone and acyclovir without any improvement.
On exam, there was no fever, malar rash, oral ulcers or active arthritis. Neurologically, she had a right
sided facial droop with tongue deviating to the right, decrease in hearing on the right, and decreased
sensation on right side of face. She had 4/5 strength and decreased sensation in both right upper and
right lower extremities. She appeared to have memory deficit.
Her labs showed only minimal elevation of the disease activity. Head CT was normal. MRI of the brain
showed an irregular elongated enhancing mass centered at the level of the floor of the fourth ventricle
with mass effect upon the posterior margin of the brainstem. The patient underwent surgery which
confirmed the diagnosis of ependymoma histologically and had subsequent resolution of neurological
symptoms.
Discussion/conclusion: SLE may present with a myriad of neurologic manifestations. One could quickly
blame neurologic symptomatology on lupus in an untreated patient. However it is still important to rule
out other organic causes. In this case, workup showed a surprising finding of an ependymoma which
could have been missed if MRI was not done. Ependymomas are glial tumors that usually grow from the
ependymal lining of the ventricular system. They account for <10% of the CNS tumors. In adults, 75% of
ependymomas arise in the spinal canal, but the ependymoma in our patient arose from the level of the
4th ventricle. Presentation sometimes includes cranial nerve palsies, but it varies depending on the
location. Treatment includes surgical resection, radiation therapy, and in some cases, chemotherapy.
[Date]
This case once again points to an importance of systematic workup of neurological symptoms and
prevention of premature closure of the diagnostic process.
196
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Deepti R Baheti, MBBS
Acute ischemic stroke secondary to reactive thromobocytosis due to iron
deficiency anemia
First Author: Deepti R Baheti, MBBS Second Author: Rupinder Singh, MD
Introduction: Literature, as early as 1965, describes reactive thrombocytosis due to iron deficiency. However the
elevation in platelet count is usually mild to moderate. Extreme thrombocytosis is rare. Reactive thrombocytosis
due to iron deficiency has been recognized as a rare cause of stroke, most of these cases being reported in
pediatric population. This is a report of a near fatal case of acute ischemic stroke secondary to extreme reactive
thrombocytosis, secondary to iron deficiency, in an otherwise healthy young man.
Case presentation: A 50 year old man presented to the emergency room within thirty minutes of developing rightsided weakness with difficulty speaking. CT scan of the head was negative for any hemorrhage. The patient was
given tissue plasminogen activator (tPA). Due to worsening aphasia while on the tPA infusion, a repeat CT scan was
performed which was unchanged, and therefore tPA infusion was resumed. CT angiogram revealed widely patent
cerebral vessels but the supraclinoid left internal carotid artery appeared to fill retrograde. A carotid ultrasound
showed a completely occluded left internal carotid artery and a thrombus in the left internal jugular vein.
An extensive work up for thrombocytosis was initiated. A 2D ECHO showed sinus tachycardia with hyperdynamic
left ventricle with no evidence of intra-cardiac vegetations or thrombi. Laboratory data revealed iron deficiency
with serum iron level of 21mcg/dl, iron saturation of 5.2% and TIBC of 402. Erythropoietin level was markedly
elevated at 293.8, in addition to a platelet count of 5,39,000/mm3 at presentation that peaked to 11,95,000/mm3
on the 20th day of hospitalization. A peripheral smear revealed leucocytosis most consistent with a reactive
process and anemia with anisopoikilocytosis and thrombocytosis. A bone marrow aspirate showed mildly
hypercellular marrow with mild megakaryocytic atypia. Studies to evaluate JAK2 V617F, JAK2, Exon 12-14
mutation, BCR-ABL1 translocation t (9; 22), MPL mutation, Factor II mutation, Factor V Leiden were all negative. He
was found to be heterozygous for MTHFR A1298C variant, however the MTHFR C677T variant was not identified. A
radiological survey for occult infective processes leading to reactive thrombocytosis was negative. It was concluded
that the thrombocytosis was secondary to iron deficiency. Intravenous iron therapy was initiated, and the patient’s
platelet count normalized in a few weeks.
[Date]
Discussion: Iron plays a crucial role as a cofactor for enzymes in the mitochondrial respiration chain, DNA synthesis
and oxygen binding in hemoglobin and myoglobin. It is also an important regulator of thrombopoeisis. Normal iron
levels are required to prevent thrombocytosis by inhibiting thrombopoeisis. In a study assaying serum level of
thrombopoietin, erythropoietin, leukemia inhibitor factor, IL-6, and IL-11 in patients with iron deficiency, only
elevated erythropoietin levels correlated with thrombocytosis, and this level decreased with iron replacement.
Reactive thrombocytosis is usually considered benign, but reactive thrombocytosis in this patient was associated
with acute ischemic stroke. Considering iron deficiency anemia as one of the risk factors for ischemic stroke and
treating it promptly may be an important step to consider in preventing stroke.
197
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Stephanie Chen, MD
A "Tear"-ible Culprit
First Author: Stephanie Chen, MD
Case: A 42-year-old man with a history of severe hypertension, chronic kidney disease (stage 3), obesity,
and active tobacco use presented with one day of acute onset abdominal pain. The pain awoke him
from sleep at 4 AM, starting in his lower back and then radiating to the epigastrium. It was constant,
severe, associated with mild nausea and anorexia, and exacerbated lying flat. His abdomen felt
distended, "like it would pop with a pin in it." Of note, he was on three anti-hypertensive medications
but had required up to five medications in the past.
Upon admission, his vitals were notable for a blood pressure of 198/101 with pulse of 76. Physical
exam showed mild epigastric tenderness. Labs were unremarkable. He had a non-contrast CT scan which
showed moderate hazy infiltration along the dilated celiac trunk extending to the bifurcation,
concerning for spontaneous celiac artery dissection. There was no bowel thickening or edema consistent
with bowel ischemia. Usually the gold standard for diagnosis of dissection is a CT angiogram, but the
risks outweighed the benefits given his chronic kidney disease. Therefore, the next day he underwent an
abdominal ultrasound with Doppler which showed significant stenosis of the celiac artery but could
not confirm dissection given the small caliber of the vessels. MRA visualized a partial occlusion of the
proximal celiac trunk 1.6 cm in length with a likely focal dissection and/or mural thrombus formation.
The patient was treated for presumed celiac artery dissection with conservative management including
bowel rest. His anti-hypertensive medications were up-titrated and smoking cessation
recommended. The next step would have been an angiogram to evaluate the need for potential stent
placement, but this was again too risky given his kidney disease. He was started on anti-coagulation to
prevent thrombosis and distal embolization. Over the next few days, he continued to have a few
episodes of pain correlated with blood pressure elevation which eventually resolved.
[Date]
Discussion: Spontaneous, isolated visceral artery dissection is rare, especially involving the celiac artery.
This patient's risk factors included atherosclerosis, hypertension, smoking, and demographics (five times
more common in males with an average age of 55). Appropriate diagnosis of this disease is essential to
prevent complications such as progressive dissection, rupture of the vessel, or aneurysm dilatation. If
the patient has no signs of bowel ischemia or bleeding, conservative treatment may be attempted
with anti-coagulation until the dissection has improved. Otherwise, endovascular therapy (i.e. stent,
thrombolytics, angioplasty) or surgery may be considered, especially if bowel infarction or arterial
rupture occurs. In conclusion, visceral artery dissection should be considered in patients
with unexplained severe abdominal pain.
198
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Jyotsna Gummadi, MBBS
MEGACOLON IN THE CHEST
First Author: Jyotsna Gummadi, MD; Nagavelli N; Vaishnav M; Suleman S. MD; Raza R. MD; Williams R.
MD, FACP
Introduction: Colonic interposition is an established procedure that has been used for replacement and
management of both benign and malignant esophageal diseases, especially if indicated for long
term. Though there is a myriad of short-term complications postoperatively, long-term complications
are rare. We present a patient with a late complication of adenocarcinoma of the transposed colon after
undergoing colonic interposition due to trauma to the esophagus from a gunshot wound.
Case: A 63 year old African American woman who had colonic interposition of the esophagus after a
gunshot wound, presented 30 years later with shortness of breath, nausea, vomiting and difficulty
swallowing for 5 days. On examination, she was noted to have distension of the anterior sternum. CT
scan showed a distended colon with possible obstruction. She subsequently underwent colonic
resection with gastric pull through and was found to have developed colon cancer of the stage T3N0M0
at distal end of the colonic interposition.
Discussion: The use of colonic grafts in patients with benign and malignant disease of the esophagus is a
technique that has been practiced for many decades. Often times, the left colon is the segment of
choice due to its anatomy, but the ascending and transverse colon can also be used. In general it is a
procedure that has been well-tolerated and thus increasing in frequency. Though, as with most
procedures of this magnitude there are bound to be postoperative complications. Occurrence of
adenocarcinoma of the transposed colon has only been described a handful of times in the literature,
yet it is something all patients who are undergoing this procedure should be screened for. Thus,
colonoscopy prior to surgery, upper endoscopy with biopsy within one year of surgery and periodic
surveillance is recommended as a preventative measure. The most common risk factors for malignant
change in interposed segments of the colon are history of colonic polyps, colitis, and family history of
colon cancer.
[Date]
Conclusion: We have described a late and rare occurrence of adenocarcinoma of the transposed colon
in our patient. This patient would likely have vastly benefited from the screening and surveillance
recommendations pre and post operatively.
199
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Samuel B Holzman, MD
Bedaquiline, a new weapon in an old war
First Author: Samuel B Holzman Second Author: Radhika Banka Third Author: Pratibh Prasad Four Author:
Zarir F. Udwadia
Introduction: While efforts over the past twenty years have led to a plateauing of incident tuberculosis (TB) cases
and have slashed associated death rates, multidrug-resistant TB (MDR-TB, defined as resistance to at least
isoniazide and rifampin) and extensively drug-resistant TB (XDR-TB, defined as MDR-TB plus resistance to any
fluoroquinolone and at least one of the three injectable second-line drugs, i.e. amikacin, kanamycin or
capreomycin) have together presented a formidable challenge. It is now thought that MDR-TB accounts for nearly
4% of new TB cases and 20% of those previously treated. The relevance of these statistics becomes apparent
when noting that treatment success rates stand at only 50-60% for MDR cases and around 40% for XDR
cases. Despite the fact that nearly one third of the world’s population is thought to be TB infected, leading to over
1 million annual deaths, the 2012 FDA approval of bedaquiline marked the first new class of anti-tubercular
medication to become available in over 40 years.
Case Description: Ms. PS is a 38-year-old housewife who first presented to the Chest Clinic at P.D. Hinduja National
Hospital in Mumbai, India in March of 2013. She had no known past medical history and her story began in 2011
when a screening chest x-ray, as part of her student visa application to the United Arab Emirates, identified
a “lesion” in her left upper lung. Asymptomatic at the time, she was placed on anti-tubercular therapy (unknown
regimen) for 2 months. About 1 year later (the Fall of 2012) she developed a dry cough. A repeat chest x-ray again
demonstrated left upper lobe disease, though with a high-normal IgE level, her symptoms were attributed to
allergic bronchitis. Antihistamines were given without improvement. Several months later Ms. PS developed
fever, fatigue and her cough became productive of copious white sputum. An acid fast bacillus (AFB) smear at that
time came back positive at 3+. No mycobacterial cultures were sent, though she was started empirically on firstline TB therapy (isoniazide, rifampin, pyrazinamide and ethambutol) as well as moxifloxacin and the injectable
aminoglycoside, kanamycin. Despite therapy, her symptoms worsened; she developed vomiting and began losing
weight. In March of 2013 she presented to Hinduja, 2.5 months after initiation of second-line therapy. Given
concern for MDR/XDR disease, additional second-line agents were empirically added (cycloserine[CS], paraaminosalacylic acid [PAS]), as well as linezolid. Final culture results showed sensitivity to only PAS, clofazimine and
linezolid. With her clinical and radiologic condition worsening Janssen was approached for compassion release of
bedaquiline (not currently approved in India), which was initiated in August of 2014 to a background regimen of
ethambutol, capreomycin, PAS, CS and linezolid. No EKG changes or other adverse events were noted after the
addition of bedaquiline and Ms. PS’s six week sputum was negative. Her cultures remain no growth to date and
she has begun to gain weight.
[Date]
Discussion: While there is still much to learn about bedaquiline, and we currently await phase III trials, there is no
doubt this agent represents a welcome step forward in the fight against global TB. A recently published phase IIb
trial showed reduced time until culture conversion with bedaquiline, though also demonstrated a small increase in
all-cause mortality, a finding that has yet to be fully explained. Despite this, as rates of resistance grow, so to will
our dependence on novel therapeutics. Udwadia and his group in India and Velayati in Iran, have both published
case series of so called “totally drug resistant TB,” essentially strains resistant to all tested first and second-line
agents, underscoring the need for further drug development, and highlighting the importance of the role
bedaquiline may soon play.
200
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Mohammad Ali Syed Jafri, MD
Acquired Frozen Shoulder: What's the "Factor"
First Author: Mohammad Ali Syed Jafri, MD Krisda Chaiyachati MD MPH Jose Castenada MD Donna
Windish MD MPH
Introduction: Acquired Hemophilia is a rare and potentially fatal bleeding disorder caused by
autoantibodies against plasma coagulation factors, commonly factor VIII, with no genetic predisposition.
Given the mortality associated with acquired hemophilia ranges from 8%-22%, it is important for every
clinician to be aware of it.
Case Summary: The patient is an 80 year-old male with history of hypertension, hypothyroidism, and
asthma who presented with left shoulder pain and easy bruising in his joints that started two days prior
to evaluation. One month before, he had two similar episodes of swelling of his right knee and right arm
with associated purplish appearing skin that resolved spontaneously after a few days. He denied any
trauma, fever, travel, or new medication. He has no family history of bleeding disorders.
On examination, patient had normal vital signs, left frozen shoulder with absent range of motion to
active or passive movements. He also had a 4x4cm hematoma on his left elbow. The remainder of his
evaluation was normal.
Work up for a possible coagulopathy revealed a hemoglobin of 9.0 (baseline 12.5, 6 months prior),
elevated PTT (46.3), low factor VIII level (3.1%, where <1% indicates severe hemophilia, 1-5% moderate,
and 5-40% mild) and high factor VIII inhibitor level (13BU, where >5BU is a high titer). The patient had a
partial response to a mixing study. ANA, RF, Hepatitis serology, FOBT, and HIV tests were all negative.
Based on the laboratory results and clinical findings, the patient was diagnosed with acquired
hemophilia. He was treated with Factor Eight Inhibitor Binding Agent (FEIBA) every 12 hours for 4 days.
He was also given cyclophosphamide and prednisone to complete a 5 week course. The patient’s
symptoms subsequently improved within one week with an associated increase in his factor VIII levels
and a decrease in factor VIII inhibitor level.
Discussion: Our patient's clinical presentation is a rare acquired condition. This autoimmune
phenomenon can occur with rheumatologic disorders, post-partum, medication induced, or is idiopathic
in 50% of cases. Treatment is aimed at controlling the bleeding and removing the inhibitor.
[Date]
Patients presenting with a high inhibitor level require the use of FEIBA, whereas patients with low
inhibitor levels can be controlled with human factor VIII concentrates. The antibodies can be eradicated
by a combination of cyclophosphamide and glucocorticoids for at least five weeks. Refractory cases may
need rituximab. Our case illustrates the classic presentation of acquired moderate severity hemophilia
with high inhibitor level, and the appropriate response to treatment. Although this is a rare case, it
highlights the importance of accurate diagnosis in combination with successful treatment.
201
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Amit A Kulkarni, MD
Untreated Hepatitis C Virus infection presenting with cryoglobulinemic vasculitis
and membranoproliferative glomerulonephritis
First Author: Amit A Kulkarni, MD, Rimoun Hakim M.D, Rudolf Pullmann M.D
Introduction: The prevalence of Type II or essential mixed cryoglobulinemia is estimated at approximately
1/00,000, although presence of cryoglobulins (CG) can be subclinical in a proportion of patients with chronic
infections. We report a classical presentation of cryoglobulinemic vasculitis and membranoproliferative
glomerulonephritis (MPGN) in a patient with chronic hepatitis C virus (HCV) infection.
Case description: A 49-year-old woman with history of intravenous drug abuse and untreated HCV infection
presented with chronic fatigue, recurrent bilateral lower extremity rash, and marked joint pain with swelling. She
was recently diagnosed with cryoglobulinemia after work up of her skin rash showed leukocytoclastic vasculitis on
skin biopsy, but was lost to follow up. Physical examination revealed palpable purpuric rash over bilateral lower
extremities. Laboratory findings were significant for elevated ESR (80 mm/hr), and renal insufficiency
(creatinine=2.8 mg/dl), while her baseline creatinine was in mid 1’s three months before the admission. Urine
studies showed hematuria and nephrotic range proteinuria (8 g/24h). Further testing revealed positive rheumatoid
factor (RF, 1:16), undetectable C4, low CH50, low-normal C3, and marked polyclonal cryoglobulinemia. HCV RNA
PCR detected high viral load (1,934,200 IU/mL). Kidney biopsy showed MPGN with mesangial sclerosis,
hypercellularity, widespread duplication of glomerular basement membrane and focal crescents.
Immunofluorescent staining was positive for IgM and electron microscopy showed sub-endothelial immune
complex deposits and foot processes effacement.
Discussion: Cryoglobulinemia is a systemic inflammatory syndrome that leads to small-to-medium vessel vasculitis
from CG-containing immune complexes. Type II or essential mixed cryoglobulinemia is largely associated with HCV
and much less frequently associated with Hepatitis B, Human Immunodeficiency or Epstein-Barr viral infections. It
is characterized by the presence of polyclonal IgG and monoclonal IgM or IgA. Type II cryoglobulinemia can
manifest as palpable purpura, arthralgias, myalgias together known as Meltzer’s triad. The predominant organs
involved are kidneys (MPGN), and nervous system (peripheral neuropathy). A disproportionately low C4 is seen in
comparison to C3. CG titers correlate with the immune complex burden, but not with symptomatology. The
diagnosis is confirmed by biopsy of an affected organ. Treatment of cryoglobulinemia is geared towards treating
the underlying disorder. Immunosuppressants or plasmapheresis can reduce the immune complex burden and are
reserved for severe consequences of cryoglobulinemia like MPGN associated with either a rapidly progressive
course or nephrotic range proteinuria.
[Date]
Conclusion: Even with wide availability of HCV antiviral therapy, Type II cryoglobulinemia should be considered in
patients presenting with typical symptoms. This case shows detrimental long-term consequences of not treating
HCV infection leading to this otherwise very preventable condition. From a clinician’s perspective, early diagnosis
and treatment of HCV and awareness of the associated conditions are needed.
202
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Ivana Milojevic, MD
Splenic infarcts in a patient with sickle cell trait and recent EBV infection
First Author: Ivana Milojevic, MD Attending: John Cmar, MD
Introduction: Symptomatic seroconversion during EBV infection or infectious mononucleosis syndrome
presents with a highly variable constellation of signs and symptoms reflecting polyclonal activation of Bcells. Patients with sickle cell trait are predisposed to occlusive crises in a variety of clinical settings, not
necessarily related to hypoxia.
Case presentation: A previously healthy 21-year-old man with a family history of sickle cell disease
presented with left flank pain and fever for several days. He was sexually active with only one female
partner and denied any history of drug abuse. His vital signs were within normal limits, except for a
temperature of 38.4 degrees Celsius. On exam, no lymphadenopathy, tonsillar exudate, or heart
murmur were detected. The left side of his abdomen was very tender to palpation but without guarding.
Laboratory data showed only mild normocytic anemia. Abdominal CT scan with oral and intravenous
contrast revealed massive splenomegaly with multiple wedge-shaped splenic infarcts.
Broad-spectrum antibiotics were started for presumed bacterial endocarditis, but transthoracic
echocardiogram did not show vegetations, and the patient remained febrile with negative blood
cultures. HIV antibody, viral hepatitis serologies, parvovirus B19 antibody, and heterophile antibody test
(Mono Spot) were negative. He further developed acute kidney injury, transaminitis, worsening anemia,
and mild coagulopathy. Peripheral smear showed anemia without specific morphologic abnormality.
Hemoglobin electrophoresis was consistent with sickle cell trait. C-reactive protein of 128.00 mg/L
(reference range <= 10.00 mg/L) and ferritin of 3,586.3 ng/mL (reference range 28.0 - 365.0 ng/mL)
confirmed severe inflammatory response, but rheumatoid factor, antinuclear antibody, typical and
atypical anti-neutrophil cytoplasmic antibodies, complement levels, serum and urine electrophoresis
with immunofixation were all within normal limits. Lupus anticoagulant was weakly positive.
Since infectious and rheumatological etiology seemed less likely at this point, malignancy workup was
pursued. Bone marrow biopsy with flow cytometry and FISH were negative. Patient underwent splenic
biopsy which showed infarcted tissue without evidence of malignancy or granulomas. Eventually, EBV
serologic panel and PCR results were available and suggestive of convalescent phase of infection.
Fortunately, there was no splenic rupture on two subsequent abdominal ultrasound examinations
performed in the setting of abdominal pain post splenic biopsy. Patient was discharged home after two
weeks, being afebrile for 48 hours, and was still feeling well on two-month follow-up.
[Date]
Discussion: Atypical presentation of EBV viral syndrome represents a diagnostic challenge and splenic
infarcts have been reported on its spectrum, although infrequently. It seems that patients with
underlying sickle cell trait are at increased risk of developing splenic infarcts, as vasoocclusive crisis
during EBV infection can be precipitated by splenic vascular congestion, transient hypercoagulable state,
or high-grade fevers, all of which were seen in our patient, in absence of hypoxia.
203
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Ivana Milojevic, MD
Have you heard of this bug? Emergence of Leclercia adecarboxylata.
First Author: Ivana Milojevic, MD Attending: John Cmar, MD
Introduction: Leclercia adecarboxylata is a ubiquitous gram negative rod found in the human digestive
tract and skin. It shares many metabolic features with Escherichia coli. With advancement of molecular
techniques, it is increasingly being recognized as a human pathogen. Infections are frequently
polymicrobial, and often occur in the setting of immunocompromise and/or trauma.
Case presentation: An 86-year-old woman with rheumatoid arthritis and osteoarthritis requiring
multiple surgeries presented with fever and infected pressure ulcer of the right heel. She had not
received any recent immunosuppressive therapy. Two months prior, she was admitted to an outside
hospital for an unspecified infection, treated with antibiotics, and subsequently spent 6 weeks in a
subacute facility. Review of systems was significant for fever, right heel pain and discharge, dry cough,
anorexia, weakness, and chronic urinary incontinence. She was febrile at 38.4 degrees Celsius,
tachycardic to 104 beats per minute, and hypotensive with a blood pressure of 95/54 mm Hg. She did
not require supplemental oxygen. Right heel exam revealed a 4.5 x 2.5 cm stage 3 pressure ulcer
with purulent discharge, surrounding erythema, warmth, and tenderness to palpation. A stage 2
pressure ulcer in the sacral area was also noted. Laboratory data showed leukocytosis of 15,030
cells/mm3 (reference range 4,000 to 11,000 cells/mm3) with neutrophilia and left shift. Chest X-ray did
not show any infiltrates. X-ray of the right foot did not show evidence of osteomyelitis or abnormal
periosteal reaction.
She received intravenous hydration and empiric piperacillin-tazobactam and vancomycin. One of two
peripheral blood cultures grew a pan-susceptible gram negative rod identified as Leclercia
adecarboxylata. The organism was presumed to have originated from the heel ulcer and caused sepsis in
our patient, as gram negative rods are rarely blood culture contaminants. The patient’s fever and
leukocytosis resolved, and antibiotics were de-escalated to oral ciprofloxacin. Repeat blood cultures
documented clearance of bacteremia. She was discharged to a subacute facility to complete 14 days of
antibiotic treatment.
[Date]
Discussion: Leclercia adecarboxylata was underrepresented as a pathogen since it was likely
misidentified as Escherichia coli until the development of more sophisticated molecular techniques.
There is a growing body of evidence supporting clinical significance of this bacterium, which was initially
isolated from wounds and more recently as a cause of bacteremia and catheter associated infections.
Organism is not necessarily opportunistic, as infections were also reported in immunocompetent
patients, although less frequently. It is usually susceptible to different antibiotics, but extended
spectrum beta-lactamase producing strains have been described in case reports. This is worrisome in
the context of frequent polymicrobial infections and potential for horizontal transfer.
204
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Nafees A Mohammed, MBBS
STEMI SECONDARY TO DIC IN THE SETTING OF PNEUMOCOCCAL SEPSIS - A
TREATMENT DILEMMA
First Author: Nafees A Mohammed, MBBS Mehwash Naseem, MD Rongras Damrongwatanasuk, MD
Rohit Gosain, MD Duncan Salmon, MD
Introduction: Disseminated Intravascular Coagulation (DIC) is a deleterious complication of infection
causing abnormal activation of the coagulation cascade. This activation produces excessive clotting and
deposition of microvascular thrombi while depleting clotting factors and predisposing to bleeding. When
these microvascular thrombi accumulate within the coronary vasculature they can cause an ST Elevation
MI. Treatment dilemmas arise when there is ongoing cardiac compromise and ischemia, but clinical
instability and excessive risk of bleeding preclude cardiac catheterization or intervention.
Case: We report the case of a 34 year old woman with history of hypertension who presented with
fevers, dyspnea, cough and sputum production. She was diagnosed with severe multilobar
pneumococcal pneumonia which deteriorated into ARDS, requiring ICU admission and intubation.
Within 24 hours her pneumococcal sepsis triggered the development of DIC with excessive bleeding
necessitating multiple red cell and platelet transfusions. She developed worsening tachycardia and EKG
changes were indicative of an inferolateral ST Elevation MI with a troponin of 11.1. Due to her excessive
bleeding, ARDS and high oxygen requirements she was at high risk of rapid decompensation with any
antiplatelet agents, heparin or cardiac catheterization and only conservative management could be
pursued. A few weeks after transfer from ICU an elective cardiac catheterization was done
demonstrating normal coronary arteries with no atherosclerotic disease. Follow up
echocardiography did not show any wall motion abnormalities and subsequent EKGs showed resolution
of ST elevation without q waves.
[Date]
Discussion: This case illustrates the complications of DIC which may precipitate multiple organ
dysfunction, and in our patient, cardiac compromise. Management of an ST elevation MI requires
emergent cardiac catheterization along with the use of antiplatelet agents and antithrobotic agents but
our patient’s instability precluded these interventions. Other case reports have noted DIC complicated
by myocardial infarction with presentations ranging from possible Legionnaires' disease to septic shock
after amniocentesis. Intervention in some of these cases still resulted in unfavourable outcomes. Due to
the possible transient nature of intracoronary microthrobi in DIC and myocardial infarction, appropriate
management of DIC and its initiating factors were given priority after assessing the risks of
deterioration. STEMI is a rare but possible complication of DIC. In other case reports procedural
intervention has not necessarily resulted in improved outcomes, and as such, conservative management
may be an effective alternative option when treating specific high risk patients.
205
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Radhika Parikh, MD
Cryptogenic Organizing Pneumonia Presenting As Recurrent Pneumonia
First Author: Radhika Parikh, MD Co-Author: Robert Hallowell, MD Faculty Reviewer: Sonye Danoff, MD
Introduction: Cryptogenic organizing pneumonia (COP) is sequelae of lung injury that often mimics bacterial
pneumonia.
Case Description: A 69 year-old man presented with one month of dry cough, malaise, and 7-pound weight
loss. He was treated empirically for CAP with 10 days of moxifloxacin; however, he was ultimately
hospitalized for fever and persistent symptoms and received additional treatment with ceftriaxone and
azithromycin. His fevers improved and he was discharged on cefpodoxime and azithromycin to complete a
10-day course of antibiotics. However, he returned to the hospital with persistent cough, non-purulent
sputum, low-grade fever, and severe shortness of breath. He has a history of mild COPD and a negative
Quantiferon test in the past. He spends a majority of his time in rural India. He quit smoking a pipe 20 years
ago. Physical exam on admission was notable for crackles at the right base and no evidence of heart failure.
He did not require oxygen supplementation. Computed tomography of the chest revealed interval worsening
of right middle and right lower lobe consolidations; sputum cultures and a comprehensive respiratory viral
panel were negative. Bronchoalveolar lavage grew only normal respiratory flora; needle biopsies of carinal
and right hilar lymph nodes revealed benign lymphoid tissue; transbronchial biopsies demonstrated focal
fibroblastic foci. He received 10 days of vancomycin and piperacillin/tazobactam and 7 days of azithromycin
with little improvement in symptoms. A video-assisted lung biopsy of the right middle and right lower lobes
was performed, demonstrating organizing bronchopneumonia without any evidence of granulomas, necrosis,
or infection. A connective tissue and rheumatoid disease work-up was negative, as were serologic tests for
HIV and hepatitis C. A diagnosis of cryptogenic organizing pneumonia was made. He was started on 1 mg/kg
of prednisone and had a rapid symptomatic improvement. He was discharged on a steroid taper with close
pulmonary follow-up and plans to repeat imaging in several weeks.
Discussion: Cryptogenic organizing pneumonia (COP) is a rare condition of the lung in which epithelial injury
is followed by “organization” or filling of the alveoli and bronchioles with loose fibroblasts in a collagen
matrix. The lung architecture is preserved and an inflammatory interstitial infiltrate is often present. The
mean age of onset is in the 6th decade of life, and typical symptoms often follow signs of an upper
respiratory infection. Cough, mild dyspnea, and fevers are common, and diagnosis is generally delayed for 12 months, with most patients receiving at least one course of antibiotics for presumed pneumonia. CT
imaging most frequently demonstrates patchy airspace consolidations, though ground glass and nodular
infiltrates are not uncommon. If diagnosed in its early stages, COP is usually highly steroid-responsive, though
a slow taper over several months is often required to prevent disease recurrence. Delay in making the
diagnosis and initiating appropriate therapy has been known to increase relapse.
[Date]
Conclusion: Clinicians should consider a diagnosis of COP in patients with suspected pneumonia that fails to
improve despite appropriate antibiotic therapy. Timely treatment with corticosteroids is effective in most
cases, though a slow taper is often required to minimize the risk of relapse.
206
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Chintan Pankaj Patel, MD
A Clean End
Chintan Patel MD MPH, Janushe Patel MD, Kenneth Remy MD.
INTRODUCTION: Alcohol based sanitizers have become a standard part of every hospital in the United
States and is mandated by the Joint Commission. The availability of these solutions also provides an
easily accessible source of intentional ingestion that could be missed while in the hospital.
CASE: A 38 year old homeless male with a history of depression, prior alcohol abuse, intravenous drug
abuse, and hepatitis C had been found lying down on a sidewalk and had admitted to alcohol and
benzodiazepine ingestion. He was brought to the emergency department for detoxification and had an
initial GCS of 15 despite being very somnolent. His initial ethyl alcohol level upon presentation was 276
mg/dl. He initially denied any suicidal ideation and was given IV hydration and multivitamins.
Approximately 10 hours later, the patient was completely awake and was uncooperative with ER
providers. When told he was to be discharged the patient stated that he was suicidal.
Approximately ten minutes later when his nurse went to check on him, he was found to have a GCS of 3
with pinpoint pupils. Multiple doses of naloxone were given with no response and the patient was
intubated for airway protection. Vital signs were within normal limits with the exception of a depressed
respiratory rate. Repeat laboratory work revealed a large anion gap metabolic acidosis and respiratory
acidosis. He was also found to have an osmolar gap of 35. A repeat alcohol level was sent out of concern
about possible ethyl alcohol ingestion and was revealed to be elevated to 521 mg/dl nearly 18 hours
after being admitted to the ER. Maryland Poison Control was contacted and dialysis was recommended
given the acute change in his mental status. After 3 hours of dialysis, his alcohol level was measured at
169 mg/dl and the patient was waking up and responding to commands. The patient was extubated
within 24 hours and when questioned admitted to committing suicide by drinking 3 cups of Purell that
he obtained by biting through the plastic container in the ER.
DISCUSSION: Acute intoxication of highly potent ethanol-based hand sanitzers can have life-threatening
consequences. Severe CNS and respiratory depression, cardiac dysrhythmias, hypotension,
hypoglycemia, and severe metabolic acidosis have all been described in severe ethanol intoxication.
Based on National Poison Data System (NPDS) data the incidence of intentional ingestion of ethanolbased hand sanitizers is increasing despite concerns of being an underreported intoxication. Typical
treatment includes supportive treatment however dialysis has been used on severe intoxications where
the patient’s neurological status was severely depressed, increasing serum osmolality, and severely
elevated alcohol levels. Purell is primarily composed of 70% ethyl-alcohol with isopropyl alcohol and
ethylene glycol as inactive, trace ingredients.
[Date]
CONCLUSIONS: Acute ingestion of ethanol-based hand sanitizers should be considered in patients under
hospital care that demonstrate acute mental status changes, especially where concerns of mental illness
may play a factor. Early identification can lead to early intervention and can potentially be life saving.
207
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Emma Sargsyan, MD
Embolic stroke: Rare Presentation of Cor Triatriatum
First Author: Emma Sargsyan, MD
Introduction: Cor triatriatum sinistrum is one of the rarest congenital cardiac anomalies, in which the left atrium
is divided into two distinct chambers by a fibromuscular membrane. While almost all patients classically present in
infancy, in very rare cases the condition remains asymptomatic until adulthood. We describe an embolic stroke as
the first manifestation of cor triatriatum sinistrum in an otherwise healthy 44-year-old man. The patient presented
with an acute onset of throbbing headache, neck pain, dizziness and blurry vision. He had no prior history of
cardiac symptoms, family history of cerebrovascular disease, nor any evidence of congenital
coagulopathy. Transesophageal echocardiography (TEE) detected a thin, mobile membrane dividing the left
atrium into two chambers, confirming the diagnosis of cor triatriatum.
Case description: An otherwise healthy 41-year old African American man presented with an acute onset of
throbbing headache, dizziness, blurry vision and neck pain, that started several hours ago. The patient denied any
prior history of cardiac symptoms, family history of cerebrovascular disease, nor any evidence of
thrombophilia. On examination, the patient was afebrile and normotensive. His physical examination including
cardiopulmonary examination was unremarkable. A chest X-ray showed no signs of heart failure and ultrasound of
the carotid arteries was normal. A computerized tomography (CT) scan of the head was within normal limits but
cerebral magnetic resonance imaging (MRI) revealed an infarction in the territory supplied by the right posterior
cerebellar artery. A complete transthoracic echocardiogram (TTE) did not reveal any significant abnormalities.
However, a subsequent transesophageal echocardiogram (TEE) clearly demonstrated a thin, mobile septum in the
left atrium. The membrane was found to have a lateral attachment above the left atrial appendage and medial
attachment in the mitraloaortic curtain, dividing the left atrium into two separate chambers. No other associated
congenital findings were seen. Inside the left atrium there was increased echocardiographic contrast. The patient’s
left atrium was enlarged. No resulting thrombi were found during the study. The surgical removal of the
membrane, as well as anticoagulation treatment with warfarin, were discussed with the patient, and the latter
option was chosen by him.
unable to detect any abnormalities, TEE showed a thin membrane dividing the left atrium into two chambers,
consistent with cor triatriatum. Cor triatriatum is a rare congenital anomaly in which the atrium is separated into
two chambers by a septated, fibromuscular membrane. It accounts for 0.1% of all congenital heart defects, with a
male:female ratio of 1.5:1. The malformation has been thought to result from anomalous growth of the septum
primum or regression of the embryonic common pulmonary vein. The severity of symptoms of cor triatriatum
depends on the degree of obstruction formed by the size, shape and number of septations of the fibromuscular
membrane as well as the resulting transmembrane flow. Untreated individuals usually die in infancy primarily due
to pulmonary hypertension secondary to compromised drainage of the pulmonary veins. When cor triatriatum is
the only abnormality, the clinical findings are similar to that of mitral stenosis, with development of pulmonary
hypertension and subsequent right ventricular hypertrophy and atrial enlargement. Almost all cases of cor
triatriatum are diagnosed in childhood and usually give rise to abnormal hemodynamics. The natural history of the
condition remains indefinite, accounting for the rarity in diagnosis in the adult population. The late onset of
symptoms can possibly be explained by the large septation of the membrane, allowing for an almost normal blood
flow towards the mitral valve. Nevertheless, it can be assumed that directly around the aperture the propagation
of the blood influx into the proximal chamber of the left atrium diminishes in the course of time. This results in
hemodynamics mimicking that seen in mitral stenosis, with increased pressure inside the left atrium. This may
[Date]
Discussion: We report the case of a 44-year-old man who presented with cardioembolic stroke. Although TTE was
208
[Date]
also explain the increased echocardiographic contrast as an indicator of greater blood echogenicity in the region of
the left atrium, demonstrated with TEE. Chimowitz and colleagues illustrate the relationship between left atrial
spontaneous echocardiographic contrast and stroke in patients with mitral stenosis. This condition results in
stagnation of blood within the left atrium and increased risk for thrombus formation. Analogous to our case, this
phenomenon may have resulted in thrombus formation in the proximal chamber of the left atrium, which leads to
embolization to the posterior inferior cerebellar artery. There are very few case reports described in literature of
cor triatriatum sinistrum in adults presenting with an embolic stroke which, including atrial fibrillation, may be the
first manifestations of this anomaly in adult life. Although only few cor triatriatum-related strokes in previously
asymptomatic individuals are referred to in the literature, almost half of these cases present with associated atrial
fibrillation and/or spontaneous left atrial ECHO contrast. Our case is one of the very first to describe this anomaly
in a patient who lacks any past contributory history and has remained asymptomatic through his adult life. Data in
the literature is extremely scarce and no widely accepted strategy is proposed to prevent atrial fibrillation and
thromboembolism in asymptomatic individuals. However, it is especially important to recognize it in adulthood
because it may be surgically correctable when hemodynamically significant.
209
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Dariush Shahsavari, MD
ZINC-DEFICIENCY ACRODERMATITIS IN A PATIENT WITH CHRONIC ALCOHOLISM
AND GASTRIC BYPASS
First Author: Dariush Shahsavari, MD Richard Williams, MD Ajoy Karikkineth, MD Zubair Ahmad,
Introduction: Acrodermatitis enteropathica is an inherited autosomal recessive disorder of jejunal zinc
absorption. Acquired cases are occasionally reported in patients with malnutrition states such as
alcoholism or malabsorptive states such as post-bariatric surgery. We report a case of acrodermatitis
enteropathica in a 39-year-old man with history of gastric bypass surgery and alcoholism.
Case: A 39-year-old male with past medical history of gastric bypass surgery and chronic alcoholism was
admitted for syncopal episode with urinary incontinence and also multiple episodes of bloody diarrhea.
Previously, the patient underwent Roux-en-Y gastric bypass in 2008 after failed lifestyle modifications in
effort to reduce body weight. Additionally in the last two and half years, the patient had abused alcohol
extensively. Skin examination showed multiple patches of dry, peeling skin on both feet. On day 5 of
admission lesions worsened to include both hands, extensor surfaces of the arms and around the mouth
which were desquamating, erythematous and painful. Serum Zinc level 0.27 mcg/mL [0.66-1.10
mcg/mL]. Skin biopsy revealed mild psoriaform hyperplasia with broad parakeratosis. The epidermis
lacked a granular layer and demonstrated spongisosis. Patient was started on a Zinc therapy (220
mg/daily) and showed gradual clearance of desquamative lesions and other symptoms on discharge.
Discussion: The role of zinc as an essential nutrient in human metabolism has been well known for
decades. The defining symptoms of hypozincemia include a classic triad of necrolytic dermatitis, diffuse
alopecia and diarrhea. It also has been implicated in delayed puberty, impaired cognition, diarrhea,
alopecia, dermatitis, immune dysfunction and delayed wound healing. Our patient suffered acquired
zinc deficiency due to two significant risk factors: alcoholism and gastric bypass surgery. There have
been several case reports of Zinc deficiency after bariatric surgeries. 324 morbidly obese patients were
reviewed retrospectively by Salle A et. al. The follow-up period was 6 months for 272 patients, 12
months for 175. 9% of patients had zinc deficiency pre-operatively but 42.5% were deficient after 1 year.
Acrodermatitis enteropathica is a papulosquamous erupting rash with well demarcated borders which
characteristically crusts, scales and eventually erodes and is associated with inherited and acquired Zinc
deficiency.
[Date]
Conclusion: The diagnosis of zinc deficiency requires a high index of suspicion in patients after bariatric
surgery due to the large overlap in symptoms amongst nutritional deficiencies.
210
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Eugene Shenderov
Systemic Lupus Erythematosus Masquerading as Ehrlichiosis.
First Author: Eugene Shenderov, Department of Internal Medicine, Johns Hopkins Bayview, Baltimore
MD.
Systemic lupus erythematosus (SLE) is an autoimmune rheumatologic disorder that often presents a
diagnostic challenge due to associated non-specific vague symptoms, the multitude of affected organ
systems, and many mimicking diseases.
A 24-year-old previously healthy African-American man with a history of childhood asthma presented to
our hospital with two months of persistent non-bloody diarrhea, nausea and vomiting, near-daily fevers,
whole body migratory arthralgias, and 30 pound weight loss. He had no history of rash. He lived in a
suburban community though he endorsed no animal or insect exposures. Otherwise, past medical,
social, and family history were unremarkable.
On presentation, the physical examination was notable for fever of 39.30C, tachycardia, dry mucous
membranes and a non-radiating systolic murmur loudest at the base. He also had a small palpable
lymph node in the left axilla that was rubbery and mobile. There was no rash or joint swelling. Labs
were notable for pancytopenia, 20% bandemia, elevated ESR of 131 mm/hr and CRP of 1.55 mg/dl (0.000.29), elevated LDH of 800 U/L (100-190), and peripheral blood smear showing 10% atypical
lymphocytes. Computed tomography of the chest, abdomen and pelvis was remarkable for
lymphadenopathy in the axillary, pelvic sidewall, and bilateral inguinal areas. A transthoracic
echocardiogram revealed no vegetations. An excisional inguinal lymph node biopsy showed no evidence
of lymphoma. An extensive workup was notable for negative rheumatoid factor, negative blood
cultures, positive ANA of >1:640, elevated gamma globulin of 2.1 (0.7-1.7), serum protein
electrophoresis consistent with acute and chronic inflammation, and positive Ehrlichia chaffeensis IgG
antibody (high titer of 1:1024). Given the constellation of symptoms, treatment with doxycycline was
commenced for human monocytic ehrlichiosis and resulted in defervescence of fevers, subjective
improvement in symptoms, and normalization of CRP. However, 4 days into the antimicrobial therapy,
his fevers recurred, and he was noted to have reddish, non-purpuric lesions on his fingertips and soles,
and a superficial ulcer of the posterior soft palate.
[Date]
Ultimately, serologic evaluation returned highly positive anti-ds DNA (titer of >1:640), with C3 and C4
hypocomplementemia, and 2 gram/day proteinuria. Ehrlichia PCR was negative. In the third week of his
inpatient stay, a renal biopsy yielded a definitive diagnosis of SLE by demonstrating histologic evidence
of lupus nephritis stage III and V with full-house immunofluorescence. He was started on corticosteroid,
mycophenolate mofetil, and hydroxychloroquine and improved significantly. This case illustrates the
diagnostic dilemma that SLE poses. It shows the importance of being cognizant of false-positive antibody
titers in the presence of active SLE-associated immune stimulation and hypergammaglobulinemia. The
patient’s presentation highlights that the differential diagnosis in a patient of any gender presenting
with lymphadenopathy, fever and weight loss must include autoimmune rheumatologic disorders,
including lupus.
211
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Ruchita Simoes, MD
STUCK BETWEEN A GIANT BULLA AND INTRACRANIAL HEMORRHAGE : AN
INNOVATIVE SOLUTION
First Author: Ruchita Simoes, MD Co-authors : MANAM R, MSIII KRIMSKY W, MD SELINGER S, MD
Introduction : Giant bullous disease is a complication of COPD, which carries a significant increase in
mortality . A bulla is considered ‘giant’ when it occupies at least 30 percent of a hemithorax. Bullectomy
has been traditionally used as the treatment and procedure of choice, albeit a highly invasive one
especially in these patients who often have significant co-morbidities. As an alternative, there are a few
case reports of Endobronchial Valves (EBV) being deployed to treat giant bulla by isolating the affected
area. We present the case of a critically ill patient who presented with intracranial hemorrhage, altered
mental status and hypercarbia who successfully underwent rapid decompression of giant bulla with
concomitant use of percutaneous tube decompression and endobronchial valves ( a combination of
procedures which, as far as we are aware, has never been attempted).
Case: A 74-year-old female with a long-standing history of COPD and sizable left apical bulla presented
with sudden onset left sided weakness. CT head showed right basal ganglia hemorrhage with mass
effect on right frontal horn. Chest X-ray and CT chest showed giant bulla in left upper lobe with
significant mediastinal deviation towards the right. As compared to previous CT chest from 4 months
ago, a significant progression of chest findings was noted. She was also found to have significant
hypercarbia. Thoracic surgery was consulted and felt that bullectomy would pose a profound risk. A
decision was made to use endobronchial valves in conjunction with percutaneous tube decompression
of the giant bulla. Patient was taken to the operating room and the left upper lobe was isolated with
bronchoscopic placement of two 7mm endobronchial valves. After confirmation of appropriate valve
placement, a 5 Fr pneumothorax catheter was inserted directly into the bulla percutaneously. Arterial
blood gas (ABG) showed immediate improvement in pO2 from 46.2 to 65.7 mm Hg and pCO2 from 63.6
to 43.4 mm Hg. The patient’s respiratory and mental status improved rapidly. She was extubated on
post op day 2 and discharged from ICU on post op day 4. At 6 month follow-up, chest Xray showed no
signs of the bulla or pneumothorax at the left lung apex.
[Date]
Discussion: Endobronchial valves are unidirectional valves, which allow for air and fluid drainage from
distal lung segments while preventing air reentry. While recent case series have reported the use of
endobronchial valves for decompression of giant bullae in high risk surgical patients, simultaneous use
of endobronchial valves and percutaneous decompression to isolate and decompress giant bullae
suggests an alternative strategy and one with the potential for a more permanent solution given the
opportunity to remove the valves once the affected area distal to them has healed.
212
MARYLAND POSTER FINALIST - CLINICAL VIGNETTE Gurkeerat Singh, MD
Cost Saving Method to Treat Loculated Parapneumonic Pleural Effusions.
First Author: Gurkeerat Singh, MD, Jessy Dhillon, MD
Introduction: Pleural infections and parapneumonic effusions commonly require drainage of infected
fluid. A 2011 RCT found that intrapleural TpA, when used with DNAase can decrease length of hospital
stay and need for surgery to treat these cases (Rahmaan and Davies et al. NEJM 2011). However,
treatment remains off-label. Our case documents the use of these therapeutic adjuncts to treat a
loculated pleural effusion in the community-hospital setting.
Case description: A 52 year old white female with a history of mild asthma presented with 1 week of
right-sided focal pleurisy and bronchitic syndrome, after failing outpatient therapy with Levaquin. She
was afebrile, without rigors, but with mild shortness of breath and cough. Chest CT showed a small to
moderate sized right-sided pleural effusion. After 48 hours of treatment with empiric antibiotics, her
pain had not resolved and the associated right- sided effusion appeared loculated. Diagnostic tap,
followed by chest tube drainage placement derived little benefit, with minimal drainage. With no clinical
improvement in 48hrs, and the possibility of the effusion being loculated based on chest CT, off-label
use of sequential TPAse and DNAse instillation into the pleural space, per the protocol established in the
RCT conducted by Rahmaan and Davies et al. (NEJM 2011) demonstrated a significant increase in chest
tube drainage from 100 cc per day to 1000 cc per day with complete resolution of patient symptoms.
Discussion: This case demonstrates that the combination of intrapleural administration of alteplase and
Dornase Alfa are useful in improving chest tube drainage in a newly-diagnosed loculated pleural
effusion, and can safely be utilized in a community hospital setting. The use of Dnase and Tpa allowed
this patient to be managed without surgery or invasive treatments, and significant cost reduction.
[Date]
Conclusion: This patient's loculated Pleural Effusion resolved with intrapleural DNAase and alteplase use
as an adjunct to chest tube drainage and antibiotics. More Randomized Controlled trials need to be
conducted to investigate fully the efficacy, dosing, and safety of intrapleural DNAase and alteplase in the
treatment of patients with this condition.
213
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Fadi Alkhatib, DO
Unmasking the Silent Infection!
First Author: Fadi Alkhatib, DO
Introduction: Cryptococcus meningitis is well described in AIDS patients. Patients with AIDS starting
HAART therapy have the potential to develop immune inflammatory response syndrome, unmasking
meningitis already present or paradoxically making symptoms worse.
Case presentation: A 30 your-old Mexican Male is presented with sub-acute progressive headache,
nausea, and vomiting for the past week. Patient has a past medical history of HIV who was started on
HAART therapy a month prior to presentation with recent CD4 count of <1. He also presented a week
earlier to the ED with similar symptoms where he had a Head CT that showed Chronic maxillary sinusitis
with no acute intracranial abnormality. He was discharged to follow up with PCP. Headache has been
deteriorating since his visit thus presented again to our institution. Headache was in the temporal
parietal region and is worse with supine position. On presentation Vital signs were stable and physical
exam was normal. Due to his progressive worsening headache patient underwent lumbar puncture.
Lumbar puncture CSF analysis showed colorless CSF with WBC count 6 /mm3, 0 RBC, 37% segment and
44% lymphocyte, 15% monocyte, 2% eosinophile, protein 38mg/dl, Glucose 45 mg/dl, and the pressure
was 8 mmHg. Pertinent CSF labs had positive Cryptococcus antigen with 1:2048 titer. Blood Cultures
were positive with Cryptococcus neoformans as well. ID was consulted and patient was started on the
appropriate therapy for fungemia and Cryptococcus meningitis with improvement of his symptoms. It
was thought that his symptoms were contributed by the Immune response inflammatory syndrome
(IRIS) as he started HAART therapy few weeks prior to presentation.
[Date]
Discussion: IRIS is a condition where the immune system begins to recover and response to a previously
acquired opportunistic infection with an overwhelming inflammatory response. IRIS has two main types.
The unmasking types, similar to our case, where an infection previously undiagnosed or silent is
unmasked with the start of HAART therapy and body starts to respond to infection. The second type is
the paradoxical type where previously treated opportunistic infection gets worse after the start of
treatment of AIDS2. IRIS should be considered when symptoms or inflammatory signs occur after recent
initiation, re-initiation of HAART that is associated with CD4 count increase or decrease in viral load after
other causes has been ruled out1. This is mostly been reported in clinical worsening and recurrence of
clinical TB and cryptococcal meningitis following initiation of therapy2.
214
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Theodora Anagnosyou, MD
Dasatinib toxicity manifesting as pericardial tamponade
First Author: Theodora Anagnostou, MD Other authors: Wei Sun, MD, Lisa Weissmann, MD,
1
Department of Medicine, Mount Auburn Hospital, Cambridge, MA
Introduction: Tyrosine Kinase Inhibitors (TKI) can lead to systemic toxicity due to differential inhibition
of TK. We present herein a case of dasatinib toxicity associated with fluid retention and cardiac
tamponade 7 years after drug initiation.
Case presentation: The patient is a 70 year-old male with Chronic Myeloid Leukemia (CML) well
controlled on 100mg dasatinib daily for 7 years who presented with dyspnea on exertion for 2 days. On
arrival to the Emergency Department he was hemodynamically stable, but tachycardic to 110 and
physical exam was remarkable for leg edema. Xray revealed small bilateral effusions and bedside
echocardiogram showed a large circumferential pericardial effusion with right atrial diastolic collapse
consistent with tamponade physiology. The patient underwent emergent pericardiocentesis and more
than 800 cc of serosanguinous fluid was drained, followed by thoracentesis. Fluid analysis was negative
for malignant cells. He was subsequently diagnosed with dasatinib toxicity and the medication was held.
On 1 week follow up, his BCR/ABL was undetectable and it was recommended that he resumes
treatment with nilotinib after 6-12 weeks.
Discussion: Dasatinib is a second generation TKI that was approved by the FDA in 2006 for the
treatment of newly diagnosed Philadelphia Chromosome positive (Ph+) CML in chronic phase, as well as
Ph+ CML that is resistant or intolerant to imatinib.
Pleural effusions occur in 10-20% of patients on dasatinib 5-28 weeks after treatment initiation and the
incidence increases with higher doses. Potential mechanisms include SRC-kinase inhibition in
lymphocytes, but immunologic mechanisms have also been proposed. Although fluid retention has more
frequently been described with imatinib, pleural effusion was more frequent with dasatinib in the
DASISION trial.
Other serious side effects include bleeding, pulmonary hypertension and interstitial lung disease, while
pericardial effusions occur in less than 1% of the patients. Development of severe toxicity mandates
discontinuation of the drug and transition to a new medication, such as nilotinib, which belongs to the
same family and is often associated with elevations in pancreatic and liver enzymes.
[Date]
This is, to our knowledge, the first case report of cardiac tamponade associated with dasatinib use and
occurring 7 years after initiation of treatment.
215
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Swati Baveja, MD
Adrenal Apoplexy: An Unusual Cause for Crisis Decision-Making
First Author: Swati Baveja, MD Additonal Authors : Nitin Trivedi , MD Dr.George Abraham ,MD ,MPH
Introduction: Tuberculosis (TB) usually affects the lungs, but virtually any other organ can be involved.
Extra-pulmonary TB accounts for about 15 to 20 percent of all cases. Atypical presentations with poor
yield of standard diagnostic tests leads to a significant delay in the diagnosis. We present a case of
primary adrenal insufficiency with precipitation of adrenal crisis brought on by the treatment of TB.
Case Description: A 45-year-old man was seen in the hospital because of a 3-month history of
abdominal distention, fatigue and weight loss. He was born in the Philippines and has been in the US for
the last 6 years. He had a positive tuberculin skin test (TST) at the time of immigration, which was
attributed to prior BCG vaccination. On examination he had significant abdominal distention due to free
fluid. A CT scan of the abdomen revealed ascites, nodular omental thickening, mesenteric and paraaortic adenopathy, with bilateral nodular adrenal enlargement. Chest radiography did not show any
abnormality. Therapeutic paracentesis revealed an exudative effusion. Acid-fast bacilli were seen on
Ziehl Nelson (ZN) stain, which was subsequently confirmed by culture as Mycobacterium tuberculosis.
He was discharged on isoniazid, rifampin, pyrazinamide and ethambutol. One month later, the patient
returned to the hospital with fatigue, severe vomiting, loss of libido and erectile dysfunction. On
examination, he had hypotension, bitemporal muscle wasting, and hyperpigmentation of his skin, oral
mucosa and nails. Laboratory investigations showed hyponatremia and hyperkalemia. The basal and
cosyntropin stimulated serum cortisol were 1.8 mcg/dL and 2 mcg/dL respectively. The diagnosis was
made of primary adrenal insufficiency most likely due to tuberculosis with exacerbation of clinical status
by rifampin. He was discharged on hydrocortisone and fludrocortisone.
[Date]
Discussion: It is very important to be attuned to the effects of rifampin and other Cyp3A4 inducers in
patients with tuberculosis because adrenal crisis may ensue due to accelerated cortisol metabolism in
patients with untreated partial adrenal insufficiency. Furthermore, in patients already on corticosteroid
replacement therapy, the dose of corticosteroid typically requires titration up when rifampin is started.
216
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Pooja Chitneni, MD
Not Your Average Case of Diabetic Heart Disease
First Author: Pooja Chitneni MD
Introduction: Diabetes is one of the fastest growing diseases in this country and the world. Metformin is
the most frequently prescribed oral anti-hyperglycemic with the well-known but rare complication of
lactic acidosis. The sequelae of Metformin associated lactic acidosis (MALA) can be quite severe with
mortality up to 30%.
Case: A 75 yo Haitian woman with a history of hypertension and diabetes mellitus type II presented to
the emergency room with nausea and vomiting. She had recently emigrated from Haiti. One week prior
she established care with a primary care physician. Blood work revealed BUN/creatinine 20/1.6, blood
sugar 551, and she was subsequently started on Metformin 1000 mg BID. In the ED, VS were T36.6 C,
HR94, BP93/56, O2 sat 98% on RA. Labs were significant for blood sugar 250, VBG 6.98/26, bicarbonate
6, AG 40, lactate 21, creatinine 10.52, K 4.3, WBC 12.1, troponin 0.986. The electrocardiogram showed
inferior ST elevation and intermittent atrial fibrillation. A bedside echo was performed which showed a
preserved left ventricular function as well as right ventricular strain. Pulmonary embolus was ruled out
on CT pulmonary angiogram. Cardiac catheterization showed diffuse three-vessel disease including
100% occlusion of the right coronary artery, which was thought to be chronic in nature.
During this time, the patient became acutely hypotensive. She required levophed and intubation. She
had initially been started on Aspirin, Clopidogrel, and a Heparin drip, but these were discontinued once
the catheterization was performed and etiology of MI was determined to be demand ischemia
secondary to vasoplegic shock from metabolic acidosis in the setting of Metformin toxicity. Due to
anuria, continuous veno-venous hemodialysis was started.
Upon extubation on hospital day 5, the team noted that the patient had left sided weakness. CT brain
and MRI brain showed evidence of new ischemic infarcts. Given the patient’s multiple medical issues,
palliative care was consulted on hospital day 6, and code status was changed to DNR/DNI. Two days
later, the patient was made comfort measures only. She died on hospital day 14 from multi-organ
failure.
[Date]
Discussion: MALA is quite rare with an incidence of < 1 case per 100,000 treated patients. The majority
of cases occur when the contraindications to Metformin use are breached – such as a decreased
creatinine clearance. MALA likely occurred due to the patient starting a high dose of Metformin with
resultant nausea and vomiting which further worsened the creatinine clearance. One documented
complication of MALA is vasoplegic shock, a subset of distributive shock, defined by high cardiac output
and low systemic vascular resistance resulting in persistent hypotension, which adds to the high
mortality and difficulty with managing this syndrome. This unfortunate case illustrates a poor outcome
when multiple organs are affected by vasoplegic shock.
217
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Adhirath Doshi, MD
Pseudohypoglycemia- Be careful !
First Author: Adhirath Doshi, MD, Adhirath Doshi, MD (Associate), Manoj Gupta, MD, Sai Aparna
Nelakanti, MD, Nitin Trivedi, MD, FACP, Department of Medicine, St. Vincent Hospital, Worcester, MA.
Introduction: Pseudo-hypoglycemia is not a clinical syndrome, but a result of artifactually low glucose
concentration due to impaired microcirculation. It is an uncommon condition, which needs to be ruled
out in case of very low finger-stick blood glucose levels without clinical features of hypogycemia.
We present a case of pseudo-hypoglycemia which emphasizes the importance of the history and clinical
examination over the numbers.
Case: An 81 year old male with a history of hypercholesterolemia, ulcerative colitis, chronic anemia,
depression, recurrent falls, atrial fibrillation and dementia presented to the emergency department with
an unwitnessed fall at the nursing home. In the ED he was asymptomatic and denied loss of
consciousness, chest pain or shortness of breath associated with the fall. His finger-stick glucose was
44mg/dl and subsequent finger-stick glucose readings ranged from 10mg/dl to 60mg/dl. He was thought
to have the fall due to hypoglycemia and was immediately treated with IV dextrose, 1mg of Glucagon
and a stress dose of glucocorticoids for consistently low finger-stick blood glucose levels.
On examination, the patient remained asymptomatic throughout the ED course. His vital signs were
stable except for a pulse of 111/min. He was found to have cyanotic and cold fingers, despite a pulse
oximetry of 97% on room air. Venous blood glucose levels were found to be in high normal – i.e., 160’s –
presumably secondary to the interventions he had received in the ED based on the finger-stick values.
As he was on chronic use of budesonide for the ulcerative colitis, studies for adrenal insufficiency were
done and were negative. He was discharged home after being observed for 24-hours for hypoglycemia,
but he remained euglycemic throughout the hospital course.
Discussion: Our patient demonstrated pseudo-hypoglycemia, likely secondary to peripheral vascular
disease (PVD). True hypoglycemic episodes are generally characterized by Whipple's triad: typical
symptoms of hypoglycemia with a low plasma glucose measured at the time of the symptoms and relief
of these symptoms when the glucose is raised to normal; none of these criteria was present. Pseudohypoglycemia associated with PVD has been previously reported and is thought to be due to a
prolonged glucose transit time secondary to the constriction of microcirculation in PVD and a
subsequently greater than usual extraction of glucose into the peripheral tissues.
[Date]
Conclusions: We report this case to increase general awareness of the potential limitations of fingerstick blood glucose measurements in patients with impaired microcirculation. Unnecessary and
potential harmful measures in the response to pseudo-hypoglycemia on finger-sticks might then be
avoided.
218
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE David Edasery, MD
“Now You See It, Now You Don’t” - Cardiac Plasmocytoma with Tamponade
First Author: David Edasery MD Second Author: Michael Viray MD Third Author: Erik Holzwanger MS4
Fourth Author: Jared Selter MD Fifth Author: Paul Berard MD Dept of Internal Medicine, St. Vincent’s
Medical Center, Bridgeport, CT
Introduction: Extramedullary plasmacytoma (EMP) involving the heart is extremely rare, and only 13
cases have been reported in literature. We report here a case of a patient with a history of
extramedullary plasmacytoma (EMP) of the right maxillary sinus and recent diagnosis of solitary
plasmacytoma of bone (SBP), who was incidentally found on transthoracic echocardiography to have a
cardiac extramedullary plasmacytoma when she developed symptoms of cardiac ischemia after
orthopedic surgery.
Case Description: A 57 year-old Caucasian female was evaluated in our institution for NSTEMI after
undergoing an ORIF in an outside hospital for a left distal humeral fracture sustained after a fall. Her
past medical history was significant for EMP involving her right maxillary sinus confirmed by biopsy 19
months prior to presentation. She had a negative work-up for systemic myeloma including bone marrow
biopsy, serum and urine electrophoresis, and skeletal survey. After completing radiation therapy, a
follow-up PET scan 9 months prior to admission demonstrated no new focus of activity. One month prior
to admission she was found to have a biopsy confirmed solitary plasmacytoma in her right proximal tibia
with an otherwise negative skeletal survey. On this admission, initial TTE revealed a large pericardial
effusion without tamponade and a large mass in the endocardium of her right ventricle extending into
the pericardium. Subsequent cardiac catheterization revealed normal coronary arteries with an LVEF of
60% as well as tamponade physiology prompting pericardiocentesis and removal of 850 cc of bloody
fluid inside the pericardial cavity. She was started on Lenalidomide, Bortezomib and Dexamethasone
with radiation treatment to her right proximal tibia. A month later, a repeat transthoracic
echocardiogram showed the absence of pericardial effusion and non-visualization of the previously
noted large right ventricular mass.
[Date]
Conclusion: Extramedullary plasmacytomas typically demonstrate excellent disease control and longterm disease free survival with radiation therapy, but approximately 25% progress to myeloma in 5
years. Based on rare cancer network data for solitary plasmacytoma of bone, up to 75% of patient may
have a monoclonal protein in urine or blood and progression to myeloma at 5 and 10 years is 51% and
72% respectively. Work-up with serum and urine protein electrophoresis, serum free light chain assay,
and plasma phenotype is important to predict progression to systemic myeloma. Although cardiac
involvement from EMP is extremely rare, it should be included in the differential diagnosis of a patient
with known history of EMP presenting with signs of cardiac ischemia.
219
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Gunjan Garg
Meloxicam Induced Acute Kidney Injury Presenting as Nephrotic Range Proteinuria
First Author: Gunjan Garg OTHER AUTHORS: Aswanth Reddy, M.D., Akhila Ramayapally, M.D., John
Littell, D.O.
Introduction: Non-steroidal anti-inflammatory drugs are one of the major causes of acute kidney injury
(AKI). It presents as acute tubular necrosis or acute interstitial nephritis. In the US it is estimated that
acute kidney injury comprises about 1% of hospital admissions. Meloxicam is an oxicam derivative with
less than 1% risk of acute kidney injury. Here we present a case of meloxicam induced AKI presenting as
nephrotic syndrome.
Case: A 56 year old woman presented with five days of progressive fever, nausea, vomiting and malaise.
These symptoms were associated with decreasing urine output. She had a recent history of sinusitis
treated with amoxicillin. Initial evaluation in the emergency department showed an elevated BUN of
105mg/dl and creatinine of 11.87mg/dl with severe metabolic acidosis (arterial pH of 6.84 and
bicarbonate of 4 mEq/l). She was admitted to the intensive care unit for emergent dialysis. Toxicological
analysis for solvents was negative. Interestingly, the urinalysis on admission showed a nephrotic range
urine protein to creatinine ratio of 3.5. Retrospective review showed that she was started on meloxicam
4 weeks prior to the hospital admission. Her home medications also included hydrochlorothiazide and
valsartan. She received one cycle of hemodialysis. Repeat urinalysis on the third day of hospitalization
showed hematuria, granular casts and mild proteinuria. At this point, the condition was consistent with
acute tubular necrosis, which was supported by granular casts in the urine. Her urine output, BUN and
creatinine improved to normal.
[Date]
Discussion: Meloxicam rarely causes acute kidney injury, and usually presents as acute tubular necrosis.
Meloxicam causing nephrotic syndrome is rare, and one case has been reported so far. Our patient
presented with nephrotic range proteinuria later manifesting as ATN. This has seldom been reported in
literature. Also the risk increases with ACE inhibitors and diuretics, as in our patient. This case
demonstrates potential toxic effects of meloxicam on renal function, albeit infrequently reported.
220
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Samaher Hashim, MD
Kikuchi Fujimoto Disease; Out of Sight and Out of Mind?
Samaher Hashim, MD (Associate), George Abraham, MD, MPH, (Fellow)
INTRODUCTION: Kikuchi-Fujimoto disease (KD) is a self-limiting condition, characterized by benign
lymphadenopathy with associated fevers and systemic symptoms. It most commonly affects adults
younger than 40 years of age and of Asian descent. The etiology is unknown, although viruses and
autoimmune mechanisms have been proposed. Diagnosis requires histopathologic examination and
exclusion of other factors by ancillary studies.
CASE PRESENTATION:A 30 year old Indian female, who immigrated to the US 12 years ago, her last
travel to India having been in 2012, presented to her primary care physician in November 2013 with
arthralgias, fevers of 102°F and increasing fatigue. She was diagnosed ‘clinically’ with ‘Strep throat’ and
was treated with multiple courses of antimicrobial agents with no relief. Further investigations including
serologies for Lyme disease were performed, although she had no epidemiological risk factors for
acquisition of disease. Antibody titers were positive without a positive Western Blot test, but she was
treated with doxycycline for 21 days and had marginal relief of her symptoms for 2 weeks. Thereafter,
she had a recurrence of symptoms in addition to increasing swelling and tenderness over the right side
of her chin, anorexia and weight loss of 10 lbs over a two week period. She was on no medication and
had no pertinent family history. Examination at admission revealed an emaciated female who was
afebrile and hemodynamically stable. She was poorly communicative due to significant discomfort in her
neck from a large matted mass in the right submental region, that was poorly mobile and not palpable in
the floor of her mouth. The rest of her examination was essentially unremarkable; specifically, no other
lymph nodes were palpable. Her laboratory work up showed the following abnormalities: WBC 2.9 (62%
neutrophils, 32% lymphocytes), LDH 614, ESR 128, ALT 85, AST 131 and ALP 206. A CT of the neck
revealed extensive lymphadenitis. A CT of the chest, ANA, PPD, HIV, CMV, EBV and parvovirus B19
serologies were negative. A lymph node biopsy revealed necrotizing histiocytic lympadenitis without
caseation, consistent with KD.
[Date]
DISCUSSION: While the pathogenesis of Kikuchi disease is unknown, the clinical presentation, course,
and histological changes suggest an immune response of T cells and histiocytes to an infectious agent.
Numerous inciting agents have been proposed, including EBV, HSV6, HSV8, HIV, parvovirus B19,
paramyxoviruses, parainfluenza virus, Yersinia enterocolitica, and Toxoplasma. While the disease is welldescribed, unless there is an index of suspicion, it can remain undiagnosed or worse, misdiagnosed for a
long time, as happened in our patient.
221
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE SAURABH JOSHI, MD
A Rare Cause of Acute Kidney Injury, Proteinuria and CKD in a Young Patient
First Author: SAURABH JOSHI, MD Second Author: Kevin Martin, MD Third Author: Hemant Magoo, MD
Fourth Author: Ashish Verma, MD
Introduction: The kidney is commonly involved in amyloidosis and is invariably involved in secondary
amyloidosis (SAM). We report a rare case of SAM due to chronic osteomyelitis and ‘skin popping,’
presenting as acute kidney injury (AKI).
Case: A 34 year-old Hispanic female with a remote history of IV drug abuse (IVDA) and left forearm and
left below-knee amputation following a motor vehicle accident (MVA), presented with deteriorating
mental status, cough and fever. She had just completed a two-week course of valacyclovir for shingles.
At presentation, her vitals were normal but she was obtunded and had crackles at the lung bases. Brain
imaging and lumbar puncture were negative, and she was empirically treated for a community-acquired
pneumonia. Creatinine at baseline was 1.5mg/dl (CKD III of unclear etiology) but increased over the next
3-4 days to 6mg/dl. She had nephrotic range proteinuria with benign urine sediment; imaging showed
normal sized kidneys without obstruction. Serum complement, ANA, ANCA, DsDNA, anti-GBM
antibodies and cryoglobulins were all negative. Kidney function did not improve for a couple of weeks,
and a kidney biopsy showed severe deposition of serum amyloid A protein (SAA) in all compartments of
the renal parenchyma, suggesting secondary amyloidosis (SAM). Creatinine stabilized at 5mg/dl, and she
was discharged home once the mental status changes, attributed to valacyclovir and narcotics, resolved.
Work up for chronic inflammatory arthritis, IBD, lymphoma and other conditions known to be associated
with SAM was negative. The history was reviewed with the patient at a follow-up clinic, and it turned
out that she never had an MVA, but rather incremental amputations for severe chronic osteomyelitis
due to ‘skin popping.’ Indeed, the IVDA-induced osteomyelitis was causative of SAM in this patient.
[Date]
Discussion: Secondary amyloidosis (SAM) is characterized by extracellular tissue deposition of fibrils of
SAA, an acute phase reactant. It is a nonspecific condition that can occur in a number of chronic
inflammatory and hereditary conditions. Chronic skin inflammation due to ‘skin popping’ is a rare cause
of SAM. Our patient’s habit led to severe chronic osteomyelitis, contributing to the pathogenesis of
SAM. The rare and unexpected presentation of SAM as AKI in this patient highlights the importance of
kidney biopsy in establishing an accurate diagnosis. It also highlights the importance of accurate history
taking and of revisiting it when the clinical findings do not correlate. This patient’s family initially denied
the true history, as they were trying to shield the patient’s young children from that information.
222
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Mariam Lotia, MD
Plasmapheresis: A Rescue Therapy in Thyroid Storm.
First Author: Mariam Lotia, MD, Reshma Abraham, MD, Zainab Basheer, MD, Nitin Trivedi, MD.FACP,
Department of Medicine, Saint Vincent Hospital, Worcester, MA
Introduction:The conventional therapy for thyroid storm consists of anti-thyroid drugs, corticosteroids,
and beta-blockers. In patients who are either intolerant or fail standard treatment, extracorporeal
plasmapheresis has been used for treating thyroid storm. We present a case report of thyroid storm
successfully treated with plasmapheresis.
Case presentation: An 85-year-old female with a history of Graves’ disease presented with 10 days of
confusion, progressive anorexia and weight loss. Review of systems was positive for watery diarrhea.
She had been on methimazole for the prior 10 years, but discontinued it two weeks prior to admission
for an anticipated radioactive iodine ablation. On physical examination vital signs showed a temperature
of 97.7°F, pulse 110, respiratory rate 18, blood pressure 129/89, and oxygen saturation 98% on room
air. Thyroid examination did not reveal lid lag, exophthalmos or any features of Graves’ disease.
Cardiovascular examination demonstrated an irregularly irregular rhythm and mild pedal edema
bilaterally. Labs revealed hypercalcemia (11.7 mg/dL), hypernatremia (147 mEq), and new-onset atrial
fibrillation on EKG. TFTs showed suppressed TSH and elevated thyroid hormone levels (see table).
Thyroid stimulating immunoglobulin was significantly elevated (657%). During hospitalization she
developed an altered sensorium. A brain CT was essentially unremarkable. The diagnosis of thyroid
storm was made based on the Burch-Wartofsky score of 55. She was initially treated in the ICU with
conventional therapy for thyroid storm, but without clinical improvement, plasmapheresis was initiated.
After two consecutive sessions of plasmapheresis, there was significant clinical and biochemical progress
(see table). The patient received rectal administration of methimazole until she was able to swallow
medications and then was subsequently switched to oral formulation.
Admission
Day of ICU transfer
Post 1st session of
plasmapheresis
Post 2nd session of
plasmapheresis
TSH µ/ml
<0.005
<0.005
0.371
Free T4 ng/dL
>7.8
4.4
2.7
Total T3 ng/dL
452
208
136
0.127
1.4
62
[Date]
Discussion: Therapeutic plasmapheresis works as a stabilizing measure in thyroid storm by removing
thyroid hormones bound to thyroxine-binding globulin. In our case dramatic clinical improvement and
rapid reduction in the levels of thyroid hormone were seen following plasmapheresis. The effect of
plasmapheresis lasts for 24 to 48 hours, providing a window of time for definitive therapy. Rectal
methimazole was transiently used as an alternative to oral formulation with an equal clinical effect.
With her excellent response to plasmapheresis, and previously published case reports, we conclude that
plasmapheresis can be used as a therapeutic option for severe thyrotoxicosis.
223
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Lucian M Neville, MD
THE UNFORGIVING TROPONIN LEAK
First Author: Lucian M Neville, MD Second Author: Fahad Alsindi, MD Third Author: Jennifer Collins, MD
Introduction: Acute Type A aortic dissection is a time-sensitive emergency with high mortality. Prompt
identification is critical and modern diagnostic imaging has greatly expedited surgical intervention. We
report an unusual case of acute Type A dissection masked by standard diagnostic imaging.
Clinical Presentation: A 54-year-old male presented to an outside hospital with severe headache
associated with non-specific chest discomfort and a systolic blood pressure of 190 mmHg. Symptoms
began after bending over to pick up a tool at work. A head CT in the emergency department showed no
abnormality; however EKG demonstrated 1-mm ST-depressions in the lateral leads. Labs were significant
for a troponin of 1.7 ng/ml and D-dimer of 773 ng/ml. CT angiogram (CTA) evaluation was negative for
pulmonary embolism and aortic dissection. In this setting, a diagnosis of non-ST elevation myocardial
infarction was made, a heparin drip was started, and he was transferred to our facility for coronary
angiography.
In our Coronary Care Unit, he denied chest pain, but complained of worsening dyspnea. Re-examination
revealed a soft diastolic murmur. An emergent transthoracic echocardiogram revealed a severely dilated
ascending aorta, with severe aortic regurgitation. Transesophageal echocardiogram confirmed a large
ascending aortic dissection at the sinotubular junction with severe aortic regurgitation.
Discussion: Acute Type A aortic dissection is a life-threatening cardiovascular emergency and in-hospital
mortality rates approach 30%. However, this statistic is far less forgiving when diagnosis is delayed.
Physical examination and plain radiographs cannot reliably exclude aortic dissection, and thus a superior
screening test is needed.
CTA allows timely, non-invasive evaluation of the aortic anatomy and excellent visualization of the
characteristic intimal flap. The sensitivity and specificity of CTA to diagnose dissection are reported as
90%. Although our patient exhibited some classic features of dissection, his diagnosis was delayed by an
initial falsely-negative imaging study. This occurred because of improper timing between contrast
injection and image capture. Premature image capture prevented the visualization of an intimal flap or
false lumen, since contrast media was yet to reach the critical area of dissection. The patient
subsequently underwent successful aortic root and valve replacement and has done well in outpatient
follow up with no complications.
[Date]
Conclusion: Acute Type A dissection is an unforgiving, life-threatening medical emergency. Despite the
reported diagnostic success of CTA, aortic dissection remains an illusive diagnosis that requires
diligence, meticulousness, and a high index of suspicion to consider the diagnosis.
224
MASSACHUSETTS POSTER FINALIST - CLINICAL VIGNETTE Erin E O'Shea, DO
An Enemy Returns: CSF Melanomatosis
First Author: Erin E O'Shea, DO Other Authors: Shradha Gupta, MD, Gary Keilson, MD and Tony Samaha,
MD
Introduction: Melanoma and lung cancer are tumors that metastasize to the leptomeninges most
frequently (23% and 11% of CSF metastasis cases respectively). A diagnosis of CSF melanomatosis
foreshadows an abysmal prognosis with a cruel natural history, as witnessed in this case. Treatment
options are limited, and the average survival from time of diagnosis is 8-12 weeks.
Case: A 40-year-old female presented with insidious onset of headache, neck pain, low back pain and
bilateral lower extremity tingling and weakness. Her past medical history was significant for
pseudotumor cerebri, obesity status post gastric bypass surgery, stage III melanoma of the neck status
post excision with neck dissection and one year of interferon treatment 7 years prior, and recent
diagnoses of follicular low-grade non-Hodgkin lymphoma and advanced high-grade neuroendocrine
tumor of the lung.
Initial examination of the optic fundi was normal, cranial nerves and strength were intact, and reflexes
were 1+ in upper extremities and bilateral patellae.
An MRI of the brain and spinal cord showed an enhancing right parietal lesion suspicious for metastatic
disease and CSF carcinomatosis filling much of the CSF space of the lumbar spinal canal. Interestingly, a
PET scan completed less than one month prior did not show CSF activity, and a CT brain done one week
prior showed no lesion.
CSF opening pressure was 27 cmH2O. Analysis was significant for gross cloudiness, 123 WBCs, 51 RBCs,
92 lymphocytes and 1425 mg/dl protein. Neither gram stain nor culture revealed bacteria.
Immunohistochemistry demonstrated tumor cells positive for Mart-1 and S-100 and negative for
synaptophysin and CD79a – consistent with metastatic melanoma. Shortly thereafter severe pain and
progressive lower extremity weakness developed. Along with complete lower extremities paralysis, she
developed diplopia, facial droop and dysphagia.
With a negative BRAF mutation she was ineligible for BRAF-inhibitors. She was too weak to tolerate
intrathecal interferon or ipilimumab. Palliation was recommended and she was discharged to hospice,
where she later died.
[Date]
Discussion: This patient is unusual in that she had three primary cancers by age 40, any of which could
have metastasized to the leptomeninges. The pattern of her malignancies was not consistent with any
known familial syndrome, she had no family history of malignancy, and she died before genetic testing
was done. The case is compounded by the fact that she had completed one year of interferon, which has
been associated with increased incidence of secondary malignancy. Unfortunately, treatment options
for leptomeningeal melanomatosis are limited, and the course of this disease is rapid and unsparing.
225
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Alexander Adams, MD
Acute Cholecystitis As Initial Presentation Of Metastatic Lobular Breast Carcinoma
First Author: Alexander Adams, MD Second Author: Shahniwaz Labana, MD Third Author: Alaeddin
Maeza, MD Supervisor: Zain Kulairi, MD
Introduction: About 1 in 8 U.S. women will develop invasive breast cancer over the course of her
lifetime with invasive lobular carcinoma being the second most common type of invasive breast
carcinoma (approximately 5-10%). Breast cancer is associated with local lymphatic spread as well has
hematogenous spread and common sites of metastasis include bone, lung, liver, and brain. However,
gastrointestinal, gynecologic, and peritoneum-retroperitoneum metastases are also possible and more
prevalent in lobular carcinoma. Metastasis to the gallbladder however is very rare and only a few
reports are available in the literature. We present a case of metastatic lobular carcinoma presenting as
acute cholecystitis 6 years after management of primary cancer.
Case: An 86 year old female presented with right sided abdominal pain for one month that has gotten
progressively worse. She also noted worsening diarrhea, nausea and vomiting. She has a past medical
history of infiltrating lobular carcinoma of the right breast status post modified right radical mastectomy
6 years prior with lymph node biopsy staged at T3 N0(i+) MX. Abdominal exam revealed diffuse
tenderness worse on the right with a positive Murphy's sign. Laboratory testing revealed a white cell
count of 13.1 Thousand/mcL with 80 % neutrophil. Biochemical tests were within normal range (ALT,
AST, ALP, Total Bilirubin, Amylase, lipase, Lactic acid). An abdominal ultrasound and CT were performed
and showed similar findings of a contracted gallbladder containing a 0.8 cm gallstone, trace
pericholecystic fluid, and a positive sonographic Murphy's sign. Surgery was consulted and the patient
underwent laparascopic cholecystectomy and the gallbladder was sent for pathology analysis. Pathology
report demonstrated metastatic malignant neoplasm resembling the lobular carcinoma from the
patients mastectomy 6 years prior that extended past the surgical margins. Tumor markers were
positive ER and PR, and HER-2 negative similar to her breast cancer 6 years prior. Patient and her family
decided to pursue comfort measures only and she was transferred to Hospice shortly thereafter. The
patient passed away a day later.
[Date]
Discussion: Metastatic breast cancer presenting as cholecystitis is a very rare phenomenon. Lobular
histotype is the most frequent breast neoplasm associated with gallbladder metastases. As a group,
invasive lobular carcinomas tend to metastasize later than invasive ductal carcinomas and spread to
unusual locations such as peritoneum, meninges, and the gastrointestinal tract. Imaging is rarely
diagnostic as seen in this case and neoplasm rarely presents with jaundice or acute abdomen. It usually
leads to symptoms of abdominal pain, mimicking acute or chronic cholecystitis. Metastatic gallbladder
involvement from a primary breast carcinoma remains rare however it appears to carry with it a very
poor prognosis. Thus, abdominal pain in a patient with a previous history of breast carcinoma should
raise suspicion of gallbladder metastasis.
226
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Sourabh Aggarwal, MBBS
All that looks like “Brugada” is not “Brugada” – Case series of Brugada phenocopy
caused by hyponatremia
Sourabh Aggarwal, Kwabena Oware Adu-Gyamfi, Yashwant Agrawal, Devin Malik, Vishal Gupta
Brugada syndrome (BS), a life-threatening channelopathy associated with reduced inward sodium
current due to dysfunctional sodium channels, is characterized by ST-segment elevation with
downsloping “coved type” (type 1) or “saddle back” (type 2) pattern in V1-V3 precordial chest leads.
Brugada phenocopy, a term describing conditions inducing Brugada-like pattern of electrocardiogram
(EKG) manifestations in patients without true BS, is an emerging condition. We describe a case series of
Brugada phenocopy with hyponatremia.
A 63 year old lady, with history of diabetes mellitus, hypertension and schizoaffective disorder, on
haloperidol, presented to ER with confusion and altered mental status. She was drinking up to 12 liters
water and 4-5 beer cans every day. Physical examination, including vitals, was unremarkable except for
confusion and disorganized thought process. Initial labs were significant for hyponatremia (Na
112mEq/L). EKG showed prolonged QTc (547ms) and “coved type” ST elevations in leads V1-V3. Cardiac
markers were within normal limits. Electrophysiological studies and left heart catheterization were
unremarkable. Her haloperidol was held and water restriction initiated. Her sodium level improved
gradually with serial EKGs showing resolution of ST elevations and QTc interval returning to normal.
A 54 year old male, with history of hypertension, presented to ER complaining of lethargy, vomiting,
anorexia and decreased fluid intake for 7 days. He denied any cardiovascular symptoms. Physical
examination was unremarkable except for signs of dehydration. Initial labs revealed significant
hyponatremia (Na 106mEq/L) with EKG showing prolonged QTc (526ms) and a “saddle back” type ST
elevation in leads V2-V3. Telemetry did not show any evidence of arrhythmia. He was fluid resuscitated
with gradual return of sodium level towards normal, and serial EKGs showing resolution of EKG findings
with improving sodium level.
[Date]
Brugada phenocopy associated with hyponatremia has been very rarely described. There have been very
few isolated case reports. This, to the best of our knowledge, is first case series of Brugada phenocopy
with hyponatremia. Sodium channel blockers are used to unmask and/or induce EKG-manifestations of
BS in susceptible patients. Electro-physiologically, hyponatremia works similarly by decreasing
electrochemical gradient and causing decreased inward current, leading to Brugada phenocopy. We
believe that reduced trans-membrane gradient was responsible for Brugada phenocopy in our patient
which was reversible and resolved with improvement in sodium levels and potentially trans-membrane
gradient. Prognostic implications of these changes are unknown, however both our patients are doing
fine till date. Management of these patients is supportive with intensive observation. Clinicians should
be aware of the association of Brugada phenocopy with hyponatremia and be vigilant for diagnosis of
true BS in case EKG findings fail to resolve with supportive management.
227
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Reem Al-Mahdawi, MD
Marijuana Induced Biliary Dyskinesia
First Author: Reem Al-Mahdawi M.D., Larry McMann M.D., Tibia Al-Wardi M.D., Maliha Naseer M.D.,
Zayd Al-Nouri M.D., Hussam Sabbagh M.D., Sarwan Kumar M.D., Zain Kulairi M.D.
Objective: Recognize that chronic marijuana usage can be an independent risk factor for biliary
dykinesia. Propose a possible mechanism based on the current literature and provide a platform for
further investigation.
Case: A 19 year old female with no significant past medical history was admitted to ourinternal medicine
service after being seen in the emergency room on two previous occasions in the prior week for
abdominal pain, nausea, diarrhea, and vomiting. She had a social history significant for daily marijuana
usage over the last 5 years. Work up during the first two presentations included a computed topography
(CT) of the abdomen which was negative. Labs were unremarkable. She was given antiemetics, narcotic
pain medication and sent home with a diagnosis of gastroenteritis
On the day of her second discharge she returned 8 hours later with severe nausea and vomiting. The
patient reported that she now had severe colicky abdominal pain. Labs and vitals were unremarkable.
Physical exam was positive for diffuse abdominal pain with palpation, worse in the right upper quadrant.
An upper endoscopy was done which showed gastritis. She continued to have nausea and pain despite
treatment. Surgery evaluation was obtained and a hepatic biliary scan was ordered. The results
demonstrated a gallbladder ejection fraction of 19%. She subsequently underwent a laparoscopic
cholecystectomy and her symptoms of pain and nausea resolved.
Discussion: Biliary dyskinesia related to cannabis use has never been reported in the literature. The
patient in the above case is the first suspected case. In a study in 2001 they looked at the effect of CB1
cannabinoid receptors in rat hippocampal slices and it’s effect on cholcystokinin (CCK) release. They
concluded that activation of the CB1 receptors in the brain lead to less release of CCK which could
contribute to learning and memory deficits. Many studies in the literature have pointed that
cannabinoid receptor activation in the gut have lead to a decrease in peristalsis. We hypothesize that
cannabinoid receptors in the gut inhibit CCK release and lead to biliary dyskinesia.
[Date]
Conclusion:Cannabis use and it’s effects on the gastrointestinal system have focused primarily on it’s
anti peristaltic properties in the gut. Research and prevalence on the biliary dykinesia associated with
cannabis has not been studied. This observation and hypothesis leads the way for a possible case series
and further study.
228
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Omar Al-Shuwaykh, MD
A Patient saved his own life-- A curious case of chest pain: Negative Dobutamine
SPECT rMPI ending up with CABG due to triple vessels disease.
First Author: Omar Al-Shuwaykh, MD, Harith Alshuwaykh, MD, Jandark Yusef, MD, Mirela Titianu, MD,
Bashar Nahab, MD, Kamal Kassem, Khalid Zakaria, MD, Sarwan Kumar, MD
Introduction: The stress test helps to diagnose coronary artery disease. Sensitivities and specificities for
stress tests are often reported as being between 70% and 90%. Patients with positive tests are more
likely to have their results verified with further testing, while those with negative tests are rarely
referred for subsequent studies. We present a case of 54-year-old male presented with chest pain, had
negative stress test but was found to have 3 vessel diseases and ended up with CABG.
Case: A 54-year-old male with a history of smoking, hyperlipidemia and a family history of early CHD;
presented with recurrent episodes of left side chest pain for the last 3 weeks, episodes last more than
20 min, 6/10 in severity, pressure in nature, radiate to the left jaw and left arm, aggravated by exertion,
partially relieved by sublingual nitroglycerine and sometimes associated with palpitations, SOB and
dizziness. He had a negative stress test 3 years ago for similar pain. EKG showed no evidence of
ischemia, 3 sets of troponins were < 0.010. Dobutamine stress SPECT rMPI done before discharge was
normal. The patient insisted to have a cardiac catheterization and was found to have diffuse 50% area of
stenosis in the left circumflex coronary, severe 80% stenosis at the proximal part of the LAD and total
occlusion at the proximal part of the RCA. The patient underwent CABG of 3 vessels.
[Date]
Discussion: Stress tests detect lesions that are greater than 70%. The performance of dobutamine SPECT
rMPI (radionuclide myocardial perfusion imaging) for the diagnosis of CHD was evaluated in a review of
1014 patients from 20 studies. The sensitivity for detecting the presence of CHD in patients with one,
two and three vessel disease was 84, 95, and 100 percent respectively. But if an individual has multiple
50% blocked arteries, you’re going to miss that on a stress test, yet that individual is likely at significant
risk for a future cardiac event. Sometimes, it appears that flipping a coin would be a more sensitive
mechanism for detecting CAD than relying on a stress test. In the CASS (Coronary Artery Surgery Study)
population, the prevalence of CHD in this group is 89% but the false negative rate of the exercise stress
test is 65%. Results of the CASS study regarding the exercise stress test could be applied to the
dobutamine SPECT rMPI.
229
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Tiba Alwardi, MD
Familial Occipital Neuralgia; Role of the sodium channels in pathogenesis
First Author: Tiba Alwardi, MD, Larry Mcmann, MD, Reem almahdawi, Khalid Zakaria, MD, Zain Kulairi, MD
Introduction: Occipital neuralgia (ON), also known as C2 neuralgia, or Arnold’s neuralgia, is a medical
condition characterized by chronic pain in the upper neck, back of the head and behind the eyes.
ON is diagnosed when the patient meet the following International Headache Society (HIS) Criteria; (1)
Paroxysmal stabbing pain, with or without persistent aching between paroxysms, in the distribution of the
greater, lesser or third occipital nerves; (2) Tenderness over the affected nerve; (3) Pain is eased temporarily
by local anaesthetic block of the nerve; (4) Pain from the alantoaxial or upper zygapophseal joints or from
tender trigger points in the neck muscles or their insertions should be ruled out.
We present a case of hereditary ON which present in a young female inherited from her mother with onset of
occurrence around the same age.
Case: A 27-year-old female with no significant medical history presented with episodes of severe intermittent
headache over the past 3 weeks. The pain is electric and stabbing in nature, 10/10 in severity, lasted 10-15
seconds, located in the right occipital region and radiates to the right scalp and cheek. Her first episode
happened while she was brushing her teeth and since then she continued to have frequent attacks of
headaches.
Family history was significant for a history of ON in her mother around the same age that was treated with
gabapentin with complete resolution of symptoms subsequently.
Physical exam was unremarkable except for tenderness over the right occipital region of the
scalp. Computed Topography of the head and neck, Magnetic Resonance Imaging of the brain and venous
system were normal. Patient was started on carbamazepine and gabapentin and she had mild relief. A
greater occipital nerve block was performed on the second day of admission, which provided complete
resolution of her symptoms. She was discharged home on carbamazepine and has been symptom free
thereafter.
Discussion: Many reports in the literature described familial cases of cranial nerves neuralgia with familial
trigeminal neuralgia being the most common. On the contrary familial ON was only reported twice.
Sodium channels play a major role in the pathogenesis of neuropathic pain since it causes derangement in
the pain threshold. For example, the gain-of-function mutation of one particular sodium channel, Nav1.7,
causes inherited erythromelalgia. This Nav1.7 mutation results in relatively large responses to small, subthreshold depolarization.
Conclusion: Further investigation of these cases may provide a better understanding of the sodium channels
role in the pathogenesis of ON and lead the way to a permanent cure in the future.
[Date]
We hypothesize that a mutation of the sodium channels is causing the familial ON specially if we know that
these patients will respond well to sodium channel blockers like carbamazepine.
230
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Mansoor A Arain, MD
A Rare Malignancy with Comorbid Hematologic Disorder
First Author: Mansoor A Arain, MD Second Author: Valerie Vaughn-Sandler, MD
A 51 year-old Chinese male with chronic sinusitis presented to the hospital with fever, altered mental
status, and persistent left-sided hemifacial pain despite having recently completed a course of
antibiotics for presumptive sinusitis. On arrival to the ER, he was febrile, tachycardic, and hypotensive.
His exam was significant for visible deformation of the left midface, redundant tissue in the left nostril,
and a penetrating ulcer through the hard palate, as well as cervical lymphadenopathy,
hepatosplenomegaly, jaundice, and confusion. His labs were notable for pancytopenia, acute kidney
injury, and hyperbilirubinemia. His ferritin level was higher than the upper limit of detection, and his
soluble interleukin 2 receptor (IL-2R) level was also elevated. Hepatitis serologies were negative, though
he was found to be Epstein-Barr virus (EBV)-positive with a significant viral load. Imaging confirmed the
presence of a nasal mass, as well as multiple fluorodeoxyglucose (FDG)-avid lesions throughout his brain
and abdomen. A biopsy helped confirm the diagnosis of extranodal nasal natural killer (NK)/T-cell
lymphoma. No bone marrow involvement was noted, but diffuse hemophagocytosis was present.
Chemotherapy and radiation were planned, but he expired shortly thereafter due to multiorgan failure.
[Date]
Extranodal nasal NK/T-cell lymphoma is a rare EBV-associated malignancy. It classically presents as a
destructive nasal mass in East Asian males who are 50 or older. It can masquerade as chronic sinusitis,
resulting in delayed diagnosis, and is a particularly aggressive malignancy with a propensity for local
extension, widespread metastasis, and rapid progression. Secondary hemophagocytic
lymphohistiocytosis (HLH) can sometimes be co-morbid in such patients.
231
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Nicholas A Battista, MD
Dysphagia Lusoria: an elusive diagnosis
First Author: Nicholas A Battista, MD Second Author: Robert Kornas, MD Third Author: Daniel
Brancheau, DO Fourth Author: Delano Small, MD
Dysphagia lusoria is a condition that causes difficulty swallowing and is often misdiagnosed or missed on
initial examination. The symptoms are attributed to an aberrant right subclavian artery that has a
retroesophageal course leading to vascular compression of the esophagus.
We present a case of dysphagia lusoria (with images) discovered in a 62 year-old female with coronary
artery disease and gastritis complaining of chronic nausea and chest pain. Despite an extensive medical
workup, including three esophagogastroduodenoscopies and computed tomography scans of the
thorax, abdomen and pelvis, magnetic resonance angiography of the abdomen and multiple
echocardiograms, the cause of her symptoms remained elusive. Prior to her diagnosis, she had a total of
twelve emergency department visits and five hospitalizations before dysphagia lusoria was discovered
by coronary computed tomography. Her coronary computed tomography revealed an anomalous origin
of the left coronary artery from the right coronary cusp with a retroaortic course in addition to the left
aortic arch exhibiting an aberrant right subclavian artery. She refused surgical intervention and elected
for a conservative approach to management.
[Date]
Certain medical comorbidities, including gastritis, coronary artery disease, angina and esophageal
spasm, can often mask or mimic this condition leading to a delay in diagnosis and treatment. Typically,
surgical treatment is the only curative option but symptoms can be controlled by specific dietary
modifications, the use of proton pump inhibitors and anti-anginal medication. Dysphagia lusoria is an
uncommon anomaly and even rarer cause of symptoms, however, when symptomatic and occurring in
conjunction with similar presenting conditions, it can create a diagnostic and treatment challenge.
232
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Christopher Begley, DO
An animal bacterium in the human heart – a case of native valve endocarditis
caused by Staphylococcus simulans in an immunocompetent patient
First Author: Christopher M Begley, DO, Akshay Amaraneni, MD, Andrew J Whipple, DO
Staphycoccus simulans is an infrequent colonizer of the human skin. It is a coagulase negative
Staphylococcus that is known to cause infection in humans. Most cases of this bacterium causing
infection are skin and soft tissue infections but rarely this can present as endocarditis. Risk factors for
colonization are exposure to animals as this is typically colonized in sheep, cattle and domestic animals.
We report a case of S. simulans endocarditis in a patient who did not report a history of exposure to
animals.
A 73-year-old man presented to the emergency department with subjective fevers and malaise. Past
medical history was significant for non-ischemic cardiomyopathy and a recently treated urinary tract
infection (UTI). Vitals were stable. On physical exam, a 3/6 systolic murmur with radiation to the axilla
was appreciated that was not reported previously. Initial laboratory data revealed no leukocytosis, but a
urinalysis was suggestive of a urinary tract infection. Blood cultures were obtained, and the patient was
initiated on oral antibiotics for presumed UTI and placed in observation. Within 12 hours, 2/2 sets of
blood cultures were positive for gram-positive cocci in clusters and ultimately speciated to show S.
simulans susceptible to Vancomycin. The patient was placed on intravenous Vancomycin. The patient
underwent transesophageal echocardiography (TEE), which showed a partially flail posterior mitral
leaflet, moderate to severe mitral regurgitation, a highly mobile mass consistent with a torn chordae
tendon and a small mobile vegetation on the aortic valve measuring 0.88 cm. The patient was evaluated
by cardiothoracic surgery, and due to the fact that he was compensated and hemodynamically stable
the decision was made to treat the patient with six weeks of intravenous vancomycin prior to evaluation
for mitral valve repair.
[Date]
S. simulans is an uncommon coagulase negative Staphylococcus and is found in animals with infrequent
human involvement. It causes mastitis in animals but can also lead to skin and soft tissue infections in
humans. In our research, we were able to find four other cases of endocarditis caused by S. simulans.
Typically, coagulase negative Staphylococci are considered to be contaminants of blood cultures.
However, in the right clinical setting (positive urine cultures and multiple positive blood cultures) it
should be taken seriously. This bacterium should be treated similar to any coagulase negative
staphylococcal infection. We elected to continue the patient on Vancomycin following discharge to a
rehab facility for six weeks. The importance of this case comes from the recognition of coagulase
negative Staphylococcus as a cause of endocarditis and bacteremia and should be diagnosed and treated
appropriately.
233
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Abeer A Berry, DO
Benign Metastasis: An Existing Contradiction
First Author: Abeer A Berry, DO Associate Second Author: Lohit Garg, MD Associate
Benign uterine leiomyomas are common pelvic tumors in females. They are differentiated from
malignant masses based on histologic findings. Some benign leiomyomas may be mistaken for
malignancies when they possess the capability to disseminate to other areas of the body. Benign
metastasizing leiomyomas (BML) is a rare condition where leiomyoma nodules are present in distant
body locations. We describe a case of BML in a fairly healthy female of reproductive age.
A 48-year-old female with a medical history of asthma, uterine leiomyomas and an ovarian cystectomy
presented to the emergency center complaining of intermittent lower abdominal pain. A CT abdomen
and pelvis revealed diverticulitis. Incidental findings of numerous, bilateral lung nodules measuring up to
8 mm, worrisome for malignancy were noted. Patient was referred to the pulmonary nodule clinic
following discharge. During her visit, patient discussed that she was previously diagnosed with asthma
but rarely required her inhaler in the past. She also admitted to increased frequency of rescue inhaler
use recently as well as the development of a non-productive cough and increased dyspnea on exertion.
Physical exam revealed normal findings. CT chest with contrast re-demonstrated the numerous nodules
with no significant change in size. Pulmonary function tests revealed a moderate to severe, reversible
airway obstruction consistent with asthma. Labs revealed a mild anemia and an elevated ESR. The
remainder of the testing including a rheumatologic and hypersensitivity pneumonitis workup was
negative. CT chest one year later revealed an increase in nodule sizes and some cavitation. A fiber-optic
bronchoscopy with bronchoalveolar lavage was nondiagnostic with negative cytology and cultures. A CTguided biopsy of a nodule demonstrated smooth muscle mesenchymal lesion consistent with BML.
Given patient's relative proximity to reaching menopause, decision was made to monitor patient and
repeat CT within 6 months. Repeat CT did not show disease progression and decision was made to avoid
surgery and hormone suppression.
[Date]
BML is a rare diagnosis that most commonly metastasizes to the lungs. It occurs in women of
reproductive age. The process of dissemination is not confirmed but theories include vascular or
lymphatic distribution and many indicate the spread may be iatrogenic since most case reports discuss
women with a previous history of gynecologic surgery, as noted with our patient. The disease is usually
asymptomatic but may present with symptoms including cough and dyspnea. Surveillance is adequate
with incidental findings but oophorectomy and medical management to reduce serum estrogen levels
are treatment options in those who present with symptomatic disease. It is imperative for clinicians to
be aware of this rare diagnosis in female patients of reproductive age in order to avoid unnecessary
workup, allow for appropriate management and disclaim concerns for malignancy.
234
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Suma Chinta, MD
Don't Be Fooled : Fever, Lymphadenopathy and Neutropenia Does Not Always
Equal Malignancy
First Author: Suma Chinta, MD
Kikuchi-Fujimoto disease, or histiocytic necrotizing lymphadenitis, is a benign, self-limiting disease of
unknown etiology more prevalent among Asians. The symptoms of fever, night sweats, cervical
lymphadenopathy seen in this disorder mimic lymphoma so awareness is essential.
Case: A 37-year-old Asian lady with no past medical history presented with bilateral tender posterior
cervical lymphadenopathy and intermittent fevers for three months. She noted chills, headache and
fatigue but no cough, night sweats or weight loss. Initially she responded to Tylenol and ibuprofen, but
the symptoms relapsed. She received a course of Augmentin for pharyngitis but did not improve.
Subsequently, on developing dysphagia a second course of Augmentin with a Medrol dose pack was
prescribed. CBC revealed neutropenia of 300/mm3, lymphopenia of 700/mm3, platelet count of 147
thousand/mm3, hemoglobin of 11.2 gm/dL. Lactate dehydrogenase was elevated, with normal ALT, AST,
ESR and C-reactive protein. Mantoux test, antinuclear antibody, rheumatoid factor, HIV, EBV and CMV
were negative. An excisional biopsy of the right cervical lymph node revealed Kikuchi disease. The
patient’s symptoms resolved and labs improved with high dose steroids.
[Date]
Discussion: Clinical presentation of KFD closely resembles that of hematologic malignancy. Clues to
differentiate this benign condition were the normal ESR, platelet and RBC levels in the face of
neutropenia, and lymphopenia. Although spontaneous recovery occurs over several months, steroids
have been used to help shorten the course.
235
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Christopher Vittorio Di Felice, MD
Shear stress - a case of microangiopathic hemolytic anemia and thrombocytopenia
secondary to idiopathic pulmonary arterial hypertension
First Author: Christopher Vittorio Di Felice, MD Stephen McGinnis, DO, Akshay Amaraneni, MD, Steven
Stone, PAC, Ross Driscoll, MD
Idiopathic pulmonary arterial hypertension (IPAH) is a rare and often fatal disease. IPAH can lead to a
number of complications including multi-organ failure. Hematologic sequela is a rare manifestation of
IPAH and its correlation with disease outcomes is poorly understood. We present a 31 year-old woman
with IPAH, who developed refractory thrombocytopenia and microangiopathic hemolytic anemia
(MAHA).
A 31 year-old woman with a three-year history of IPAH was admitted with acute onset of hemoptysis
and hypoxic respiratory failure. Her IPAH was managed with a continuous epoprostenol infusion through
a central venous access device. She was found to be thrombocytopenic (29,000) and anemic (9.5
mg/dL). She also had a supratherapeutic INR (5.6) due to her vitamin K antagonist. Her coagulopathy
was reversed with vitamin K. Computed Tomography (CT) angiography of the chest was negative for
pulmonary embolism but noted bilateral infiltrates. Levofloxacin was initiated for Mycoplasma
pneumoniae pneumonia with positive IgM titer. Further work-up included direct anti-globulin testing,
cold agglutinin antibody, supercoombs, PNH flow, ADAMST13, ANA, beta2 Glycoprotein, anti-cardiolipin
antibody, acute hepatitis panel and HIV, which were all negative. Her haptoglobin was low, LDH was
high and bilirubin was elevated. A bone marrow biopsy showed hyperplasia without atypical cells.
Transthoracic echocardiogram showed severe progression of her pulmonary hypertension with
pulmonary systolic pressure estimated to be 114 mmHg. Despite an exhaustive work-up and multiple
blood product transfusions, she showed signs of multi-organ dysfunction. The patient’s
thrombocytopenia was not thought to be related to her IPAH. However, it did not improve despite
systemic steroid or IV Immunoglobulin therapy. The patient was transferred to a tertiary care center
with a working diagnosis of severe progressive pulmonary hypertension with resulting microangiopathic
hemolytic anemia and associated thrombocytopenia. Ultimately, she went into acute right-sided cardiac
failure and shock leading to cardiac arrest. Resuscitative measures were unsuccessful and the patient
died. A full autopsy was declined at time of death.
[Date]
This case illustrates the significance and prognostic implications of hematologic abnormalities in IPAH.
There have been six case reports suggesting an association between IPAH, thrombocytopenia, and
MAHA. Similar to our efforts, these patients were worked up extensively to exclude other potential
etiologies. Lung biopsies in reported cases showed plexiform lesions within the pulmonary vasculature
presumed to cause mechanical destruction of red blood cells and platelets. These lesions are
representative of endothelial cell proliferation and intimal remodeling predominately seen in severe
subtypes of PAH. Further studies are necessary to validate the association of hematologic complications
and increased disease severity of IPAH.
236
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Kelly Downey, MD
Where is That Blood Coming From? And Why? Pseudohemoptysis as Presentation
of Acute Human Immunodeficiency Virus Infection
First Author: Kelly Downey, MD Leonard Johnson, MD FACP
Introduction: Expectoration of blood or bloody secretion can often be clinically challenging to
diagnose. Acute HIV has a broad array of signs and symptoms, ranging from aymptomatic to
classic acute viral syndrome (constitutional symptoms, myalgias, adenopathy). While cytopenias
are well described with acute viral infections, there is rarely concomitant spontaneous bleeding.
We present a case of apparent upper airway bleeding as the initial presentation of acute
retrovirus infection.
Case: A 23 year old man with a history of asthma and cerebral aneurysm presented with a
several day history of subjective fever, generalized myalgias, sore throat and diarrhea. One day
prior to presentation, he developed copious expectoration of bloody secretions. He described a
draining sensation in the back of his throat followed by spitting up approximately 50mL of blood
multiple times but denied vomiting or cough. Physical exam showed cervical adenopathy,
enlarged, erythematous tonsils and splenomegaly. Initial workup up showed a new leukopenia,
thrombocytopenia, and monocytosis. Monospot test, rapid influenza and blood cultures were
negative and there was no coagulopathy. Contrast CT of the thorax was unremarkable and CT of
the neck demonstrated enlarged cervical nodes with tonsillar enlargement. Bedside video exam
showed enlarged tonsils with visible vessels but no active bleeding. HIV antibody was
indeterminate (positive p24 antigen, negative HIV-1/2 antibodies). The patient improved with
supportive care. Follow-up testing revealed an HIV RNA of 510,000 copies/mL. One week
later, his bloody expectorations resolved and leukocyte and platelet counts had normalized.
[Date]
Conclusion: The manifestations of acute HIV infection are widely variable and bloody
expectoration is not described as a presenting symptoms. Hemorrhagic tonsillitis should be
added to the range of syndromes associated with acute HIV infection.
237
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE E. Ethan Ebner, DO
Minocycline-induced hyperpigmentation of aorta and aortic valve
First Author: E. Ethan Ebner, DO Second Authors: Christopher Begley, DO Alphonse Delucia, MD
Minocycline-induced hyperpigmentation is an unusual but well described phenomenon occurring after
prolonged courses of this tetracycline antibiotic. We describe a 56 year old male on minocycline therapy
admitted originally with embolic CVA, found to have an aortic fibroadenoma. He underwent open heart
surgery for fibroadenoma removal, during which he was found to have a blue, hyperpigmented aortic
valve and aorta. Given that on initial intake he was also found to have hyperpigmented blue fingernails,
these phenomena was attributed to prolonged minocycline therapy (see pictures).
A 56 year old male presented for evaluation of increasing confusion and memory loss, found to have
multiple cerebrovascular non-hemorrhagic lacunar and pontine infarcts on CT. A 2D transthoracic
echocardiogram was performed, which showed a 1cm fibroelastoma on the non-coronary aortic cusp.
This fibroelastoma was thought to be the source of embolic cerebrovascular events. Due to this finding
combined with progressive coronary artery disease, the patient was taken to the operating room for
open excision of the fibroelastoma and coronary artery bypass grafting. During the operation the patient
was noted incidentally to have a blue/gray discoloration of his aorta and aortic valve leaflets. To the
casual observer this had the appearance of an aortic dissection, but on further examination the aorta
was otherwise normal. Given that the patient also had the more commonly described finding of blue
fingernails, the aortic finding were consistent with minocycline-induced hyperpigmentation.
Minocycline is a tetracycline antibiotic that is most commonly used to treat acne vulgaris, sometimes
with years of suppressive therapy. A well-documented but unusual side effect of minocycline is a striking
blue hyperpigmentation of various tissues. It occurs most commonly in the skin, lips, teeth, gingiva,
conjunctiva, and sclera (1), yet has been documented in cardiac tissues (3,4,5,6). There are three types
of hyperpigmentation patterns seen with minocycline therapy. The first consists of blue-gray
pigmentation in areas of previous inflammation, such as facial acne scars. The second type occurs when
metabolites of minocycline are deposited in the skin of the forearms and shins (1,2). The third type is
also called “dirty skin syndrome,” consisting of brown discoloration in sun-exposed areas. The fourth
type is also due to melanin overproduction, but occurs in scar tissue (1,2).
[Date]
Our patient chose to continue his minocycline therapy due to the beneficial effects on his skin condition,
and the relatively limited visible side effects. There have been no reported consequences of aortic
hyperpigmentation in the literature. Given the histological deposition of minocycline metabolite
deposits, this phenomenon may theoretically affect intimal tensile strength. This case demonstrates an
unusual cardiac sequelae of minocycline therapy, and prompts a useful review of the more commonly
seen discoloration of dermatological tissues.
238
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE John Samuel Fleming, DO
Morphea: A rare dermatologic finding that may signal the presence of other
autoimmune conditions
First Author: John Fleming, DO Sandeep Patri, MD Brian Hays, DO
Introduction: Morphea also known as localized scleroderma is an idiopathic inflammatory connective
tissue disorder characterized by inflammation and sclerosis of the skin. The incidence is approximately 3
per 100,000 people. It more commonly affects Caucasians and females. Approximately 30% of patients
with Morphea also have other autoimmune syndromes or connective tissue disorders. There are four
types of Morphea: circumscribed, deep, generalized, and linear morphea. Circumscribed is the most
common form in the adult. It presents as single or multiple plaques often oval or round in shape. We
are reporting an interesting case of morphea.
Case Report: We describe the case of a 67 year old African American female who presented with
burning mouth pain, severe fatigue, and dryness with itching of her eyes and mouth. She also
complained of an itchy rash present for 2 years for which she had been prescribed multiple antifungal
and OTC creams which provided no relief. Examination revealed a hyperpigmented velvety rash over
the chest, beneath the breasts, and in the intertriginious areas of her groin consistent with plaque type
morphea. She also had another oval macular lesion on her right posterior arm. Most of her major
presenting symptoms were the result of folate deficiency secondary to poor oral intake and chronic
alcohol abuse. These symptoms resolved with vitamin supplementation. Our patient exhibited sicca
symptoms consistent with Sjogrens syndrome and was found to be positive for ANA(1:640), Anti SSA(81) and SS-B(18), and Scl-70(84).
[Date]
Discussion: The presentation of morphea in our patient was notable for several reasons. It is less
commonly seen in African Americans. Recent studies have shown marked delays in the diagnosis of
morphea which is most responsive to treatment during the early active stage. Our patient did already
have one lesion in the inactive stage at the time of diagnosis with post-inflammatory hyperpigmentation
which is typically unresponsive to treatment. She also had Sicca symptoms , oral ulcerations due to
vitamin deficiencies, and multiple positive auto antibodies confounding the clinical picture. Positive SCL
70 is highly specific for systemic sclerosis of which she did not exhibit any symptoms. Anti SS-A and SS-B
were also positive which together with sicca symptoms was highly suggestive of Sjogrens
syndrome. This patient is being worked up for possible undifferentiated connective tissue disease in our
rheumatology clinic. Morphea is an uncommon dermatologic autoimmune condition. When it is
discovered it should be treated promptly and further diagnostic testing should be performed to
elucidate other possible autoimmune conditions that may be contributing to a patient’s symptoms.
239
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Adam Forman, MD
Managing A Case Of Limbic Encephalitis
First Author: Adam Forman, MD Feras Bashir MD, Gaurav Chand DO
Introduction: Limbic encephalitis is a rare paraneoplastic syndrome associated with small cell lung caner
that presents with rapidly progressive focal neurologic deficits. Anterograde amnesia is a hallmark of
this condition.
Case Presentation: A 53 year old female presented to the ED with worsening cough. Chest x-ray
revealed a left upper lobe mass, which was biopsied with a diagnosis of small cell carcinoma. The
patient was started on chemotherapy with Cisplatin and Etoposide. Two weeks later, the patient
presented to her oncologist with severe anterograde amnesia and psychosis. MRI is obtained shows
bilateral enhancement of the temporal lobes not consistent with metastatic disease. Lumbar puncture
shows normal cellularity, mildly increased protein, and normal glucose. On suspicion for Limbic
Encephelitis, samples of CSF were sent to Mayo Clinic for analysis. Results came back positive for AntiHu Antibodies, diagnostic for limbic encephalitis. The patient improved with chemotherapy. Rixtuximab
was consider but witheld has the patient's status declined. She was eventually transferred to hospice
care.
[Date]
Discussion: Paraneoplastic neurologic syndromes occur in less than 0.01% of cancers, mostly small cell
carcinoma. However, they are likely under-diagnosed. Many times a diagnosis of limbic encephalitis
can precede a diagnosis of malignancy. Treatment is based on small case reports and not
standardized. The goal is to reduce tumor burden and therefore immunogenic response. Rituxan has
been showed to lead to improvement by depleting circulating B-Cells and decreasing immune
response. A high degree of suspicion is needed to establish a diagnosis. Small cell carcimonas of the
lung with paraneoplastic syndromes have a better prognosis than those without.
240
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Ayman Founas, DO
A Rare Case of Encephalopathy Induced by Metronidazole
First Author: Ayman Founas, DO Second Aurthor: Jaimin Patel, DO Third Author: Jacqueline Moore, DO
Fourth Author: Niluka Weerakoon, MD Fifth Author: Wilma Agnello-Dimitrijevic, MD
Introduction: Metronidazole is an antibiotic used for its anaerobic coverage. Known side effects include
headache, nausea, dry mouth and metallic taste. Less frequent side effects include vomiting, diarrhea,
weakness, dizziness, rash, dysuria, vertigo, paresthesias, and neutropenia. Case reports have described
rare neurologic toxicities including encephalopathy, seizures and peripheral neuropathy with
metronidazole. We present a case of reversible encephalopathy related to metronidazole toxicity.
Case Presentation: A 70-year-old Caucasian woman presented with dysarthria and confusion. Relevant
past medical history included transient ischemic attack and recurrent intra-abdominal abscesses with
fistula formation requiring chronic antibiotic therapy. She was discharged from the hospital four weeks
prior with intravenous metronidazole and ceftaroline secondary to an intra-abdominal infection.
Neurological examination revealed dysarthria with decreased deep tendon reflexes bilaterally.
Computed tomography and magnetic resonance imaging (MRI) of the brain without contrast did not
reveal any acute process. Over the next eight days, her dysarthria markedly worsened and she
developed diplopia. Electromyography and acetylcholine receptor antibodies were negative. A repeat
MRI of the brain with and without contrast was performed eight days after presentation because a
second neurology opinion was requested. Imaging displayed hyperintense signals in the bilateral
dentate nuclei and involvement of the splenium of the corpus callosum consistent with metronidazoleinduced encephalopathy (MIE). Metronidazole was immediately discontinued and the patient had a
gradual reversal of symptoms.
[Date]
Discussion: Imaging findings of metronidazole-induced encephalopathy have displayed hyperintense
signals in the bilateral dentate nuclei and splenium of the corpus callosum. Lesions are described as nonenhancing, hyperintense on T2-weighted and fluid-attenuated inversion recovery images. Rapid
discontinuation of the drug has been shown to lead to resolution of neurologic symptoms when there
are no other identifiable culprits. In our case, metronidazole was given for 44 days with a cumulative
dose of 66g intravenous and orally. The duration of treatment is shown to be variable before cerebellar
symptoms manifest and doses range from 25g to 110g. Proposed pathophysiology of metronidazoleinduced encephalopathy includes a reversible process of axonal swelling with increased water content.
Other considerations include incorporation of metronidazole into a thiamine analogue, which inhibits
phosphorylation of thiamine. This leads to reduction of thiamine absorption in the gut causing
neurotoxicity.The differential diagnosis included cerebrovascular accident, myasthenia gravis,
Wernicke’s encephalopathy, methyl bromide intoxication, maple syrup urine disease, enteroviral
encephalomyelitis and finally drug-induced encephalopathy. Her clinical history, MRI findings, and
resolution of symptoms upon discontinuation of metronidazole made us favor MIE as a diagnosis.
Metronidazole is a vastly used antibiotic and it is the role of the astute physician to keep MIE in the
differential diagnosis of patients presenting with an acute neurologic dysfunction.
241
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Lohit Garg, MD
Asymptomatic Colonic Ulceration in an Immunocompromised Patient
First Author: Lohit Garg, MD Abeer Berry, DO Treta Purohit, MD
Histoplasmosis is an endemic mycosis prevalent in areas of upper Mississippi and Ohio river valleys.
Histoplasmosis most commonly causes infection of the lungs but occasionally can infect other organs
prominently in immunocompromised patient.
A 51-year-old Laotian female with a PMH significant for systemic lupus erythematosus on steroids and
mycophenolate mofetil, ESRD on hemodialysis presented for a routine screening colonoscopy for being
above 50 years of age. Patient was completely asymptomatic denying constitutional, respiratory or
gastrointestinal related symptoms. Physical exam was unremarkable. Patient underwent a colonoscopy
that revealed a submucosal and ulcerated 3 centimeter mass in the distal ascending colon that was
biopsied. CT of the abdomen revealed abnormal wall thickening of the ascending colon consistent with
infectious colitis. The biopsy revealed granulomatous inflammation and ulceration of the colonic mucosa
with Grocott’s methenamine silver stain revealed Histoplasma. There was no evidence of other organ
involvement. She was treated for isolated gastrointestinal histoplasmosis with itraconazole once daily
for 6 month duration. Repeat colonoscopy was done after 6 month of anti-fungals and showed normal
colonic mucosa.
[Date]
Disseminated histoplasmosis can involve several systems including the gastrointestinal, skin and central
nervous system. At autopsy, about 70 percent of patients with disseminated histoplasmosis have
gastrointestinal manifestations. Clinically, however, history and physical exam are typically benign
leading to only 10 percent of the cases actually being identified. H. capsulatum gastrointestinal lesions
consist of ulcerations or polypoid masses most commonly located in the ileocecal region due to
abundance of lymphoid tissue. These lesions are usually misdiagnosed as Crohn’s disease, ulcerative
colitis or malignancy. It is important for clinicians to have a high suspicion for histoplasmosis as an
etiology especially when the patient is febrile, immunocompromised, from an endemic region or with a
history of possible exposure to H. capsulatum. Misdiagnosing the lesion as inflammatory bowel disease
will result in incorrect initiation of harmful cytotoxic agents and possible dissemination of
histoplasmosis.
242
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Jon T Golenbiewski, DO
Azithromycin-Induced Torsade de Pointes: A Rare but Real Risk
First Author: Jon T Golenbiewski, DO Second Author: Rami Khoury-Abdulla, MD
Azithromycin is one of the most commonly prescribed antibiotics, accounting for more than 51 million
prescriptions in 2013 alone. While generally safe and effective, it has been associated with QT interval
prolongation. A prolonged QT interval places one at increased risk for developing a potentially fatal
arrhythmia known as torsade de pointes.
A 65 year old female presented with a chief complaint of fatigue and progressive, non-productive cough
of 3 weeks duration. She had no past cardiac history. Family history was negative for QT prolongation,
arrhythmia and sudden cardiac death. Physical exam revealed diffuse, bilateral rales with occasional
wheezes. Vitals showed the patient to be hypoxemic, tachycardic and tachypneic. A chest x-ray showed
diffuse left sided airspace disease and a focal right upper lung opacity. She was started on ceftriaxone
and intravenous azithromycin for presumed community acquired pneumonia.
The patient developed a run of polymorphic ventricular tachycardia consistent with torsade de pointes
approximately 12 hours after receiving antibiotics. An EKG revealed a prolonged QTc of 604, elevated
from a baseline of 526 on presentation. Magnesium was administered immediately. A stat electrolyte
panel revealed no abnormalities other than a minimally decreased potassium. Shortly after, the patient
developed sustained torsade and cardiac arrest. CPR was initiated. Spontaneous return of circulation
was achieved after a cycle of chest compressions with defibrillation. Azithromycin was immediately
discontinued. The patient was treated for pulmonary tuberculosis, supported by CT findings of a 3.8 cm
left lower lobe cavitation and positive sputum AFB smear and culture. Daily EKG’s were obtained, in
addition to ongoing medication review and careful electrolyte monitoring. The QT interval remained
prolonged at a baseline of 530 throughout the course of stay. The patient had a lengthy hospitalization
but ultimately made a full recovery.
[Date]
This case emphasizes the important implications of prescribing QT prolonging agents. Despite receiving
only one dose of azithromycin, a widely prescribed drug, the patient developed a potentially deadly
arrhythmia. Identification of QT prolonging risk factors is paramount to preventing this deadly
complication. Age, female gender, hypokalemia and a prolonged baseline QT interval placed our patient
at an increased risk for QT prolongation and potential cardiovascular death. Alternative agents and QT
surveillance should be considered in such patients, as well as correction of modifiable risk factors.
243
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Maulik Govani, MD
A Rare Case of Recurrent Isolated Sleep Paralysis
First Author: Maulik Govani MD Hima Challa MD, Jared Alberts MD, Ali Shukr MD, Abdel-qader Albashabsheh MD, Naganath Thota MD
Introduction: Isolated Sleep paralysis is a phenomenon in which a person, either falling asleep or
awakening, temporarily experiences an inability to move, speak or react. It has two major classifications
Isolated Sleep Paralysis(ISP) and Recurrent isolated sleep paralysis(RISP). Hypnagogic and hypnopompic
visions are symptoms commonly experienced during episodes of sleep paralysis. Sleep paralysis has
been linked to disorders such as narcolepsy, migraines, anxiety disorders, and obstructive sleep apnea;
however, it can also occur in isolation. We are presenting this case because the prevalence of cases with
RISP as seen in our patient is thought to be uncommon.
Case: Patient is a 54 year old gentleman with a past history of OSA (non compliant with CPAP), daytime
fatigue, HTN and tobacco abuse who presented for inability to move for 20 minutes after awakening. He
mentioned this has been going on for the last 3 months with a total of 7 episodes. He denied visual or
auditory hallucinations. Although one of his stated complaints was excessive daytime sleepiness, his
Epworth Sleepiness Scale score was only 8/24. His average nocturnal sleep time was around 5-6 hours
with occasional daytime naps. He denied any history of Psychiatric disorders, Narcolepsy, Cataplexy or
RLS. He denied any alcohol or recreational drug use. He denied any family history of sleep or psychiatric
illnesses. Examination revealed an obese male in no distress. Blood pressure was 200/101 mm Hg; pulse
was 80 beats/min and regular; height was 5 feet 11 inches; and weight was 270 pounds. Upper airway
exam revealed a patent upper airway with intact tonsils. Neck circumference was close to 20 inches.
Cardiopulmonary exam revealed no abnormalities. He was alert and fully oriented with proper thought
process. Affect was slightly anxious. Basic Lab-work and CT scan of the head on admission was
inconclusive. Since this is a diagnosis of exclusion and symptomology patient was diagnosed with RISP.
Patient was advised to keep a sleep diary to record events and started on Citalopram and Alprazolam.
He was to follow up with a Sleep specialist and advised to be compliant with CPAP, which did reduce his
frequency and duration of ISP eventually.
[Date]
Discussion: Since we ruled out other possible conditions the pathogenesis in our patient was mostly
likely due to noncompliance with CPAP. Treatment of sleep paralysis is aimed at whatever causes it to
occur. Sleep deprivation, underlying psychiatric disorders(Anxiety, Bipolar, PTSD)and conditions such as
OSA are most common causes, which can be controlled with medications. Serotonergic agents may
reduce the frequency of episodes. Sleep specialist or psychiatry consultation is recommended.
244
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Hamza Hashmi, MD
'Recognising these signs will save lives'..Classical signs of a catastrophic syndrome
First Author: HAMZA HASHMI, MD Mimi Emig, MD Zubair Afzal, MD
Ehlers Danlos Syndrome (EDS) type IV is a rare connective tissue disorder that affects skin, visceral and
vascular tissue. Diagnosis is often difficult and delayed given absence of hallmark features of typical
EDS. Early recognition of characteristic skin findings may help identify serious and potentially fatal
complications.
A 19 years old male with no significant past medical history except for a recent spontaneous sigmoid
perforation five months prior to admission presented with sudden onset of lower abdominal pain. Initial
CT abdomen showed left sided retroperitoneal hematoma. Despite stable initial vitals and labs, the
patient continued to have worsening abdominal pain, developed hemodynamic instability and
eventually had pulseless electrical activity arrest. Repeat labs revealed precipitous drop in hemoglobin
and rise in serum lactate level. Repeat CT abdomen showed bilateral retroperitoneal hematomas.
Patient was aggressively resuscitated with blood and plasma products. Emergent abdominal Angiogram
revealed 23 mm aneurysmal dilatation in infrarenal abdominal aorta. An IR guided intra aortic inflatable
balloon was placed to secure hemostasis but before an aortic stent graft could be advanced the tissue
paper thin friable vessel wall started disintegrating. As aorta was considered non salvageable at this
point, the patient was made comfort care and passed away within 12 hours of admission. Autopsy
revealed typical facies with protruding eyes, thin nose and lips and sunken cheeks; a translucent skin
with prominent veins and transmural dissection of abdominal aorta. Genetic testing revealed classical
COL 3A1 missense mutation.
[Date]
Given the absence of distinct features of hyperextensible skin and hypermobile joints commonly seen in
other types of EDS, diagnosis is often difficult and delayed in a particular case of vascular EDS.
Knowledge of characteristic findings of an acrogeric facial appearance, easy bruising and thin skin with
prominent veins is a helpful tool for early diagnosis and appropriate management of subsequent fatal
complications. In the absence of specific treatment options, medical intervention should be focused on
symptomatic and prophylactic measures. Bowel perforation is managed with a conservative approach
and minimally invasive endovascular therapy is usually recommended for arterial rupture. IUDs
are contraindicated in young females and pregnant women are advised against spontaneous vaginal
delivery. After a positive test for one family member, all family members need genetic as well
reproductive counseling by a clinical geneticist.
245
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Khatri C Narayan, MBBS
A rare and interesting cause of Recurrent Pancreatitis
First Author: Narayan K C, MBBS Siddhartha Yadav, MBBS
Recurrent acute pancreatitis is often encountered in clinical practice which commonly results from
alcohol abuse or gallstones but, at times, it may not be very clear. In such cases further investigations
may be required to discern the underlying etiology.
A 26 year old female presented with abdominal pain for 7 days. Her past medical history was significant
for two prior episode of pancreatitis in the past 2 months without any identifiable cause which resolved
with conservative treatment. She denied any history of alcohol abuse or family history of pancreatitis.
On physical examination, she had significant abdominal tenderness. Complete blood count, electrolyte
panel, lipid panel, renal function tests and liver function tests were unremarkable. Her lipase was 4090 U
at presentation. US abdomen did not show any gallstone. MRCP was positive for acute pancreatitis
changes without any signs of pancreatic necrosis, cyst or anatomic changes like divisum. Serum IgG
levels were normal. Endoscopic Ultrasound was suggestive of resolving pancreatitis without any sign of
biliary sludge or stone. She underwent upper gastro-intestinal endoscopy which was unremarkable.
However, biopsy from the duodenal mucosa returned positive for celiac disease. Serum transglutamase
was 108.2 units. She was then treated with strict gluten free diet. After initiation of gluten free diet her
tTG levels have normalized. She has not had any further episodes of recurrences of pancreatitis.
[Date]
Celiac disease is a common and treatable condition that can present with atypical symptoms. One such
rare presentation of celiac disease is recurrent acute pancreatitis. Studies have shown a two to three
fold increase in risk of pancreatitis with celiac disease. This has been attributed to immunopathogenetic
mechanisms which have not been clearly understood at this time. This case highlights that celiac disease
should be considered in the etiology of the recurrent pancreatitis when the etiology is not very clear.
246
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Adnan Kassier, MD
Common Variable Immunodeficiency Complicated by a Lymphoproliferative
Disorder
First Author: Adnan Kassier, MD, member, Carl Lauter, MD, MACP, Reba Johnson, MD, William
Beaumont Hospital, Royal Oak, Michigan, Oakland University William Beaumont School of Medicine,
Rochester Hills, Michigan
Hypogammaglobulinemia can have different etiologies. It could be caused by medication or associated
with an underlying lymphoproliferative disorder. Common variable immunodeficiency (CVID) is a
primary immunodeficiency disorder characterized by impaired B cell and T cell dysfunction and defective
immunoglobulin production. There is an increased risk of malignancies in patients with CVID, nonHodgkin’s lymphomas being the most common. Increased awareness and cancer surveillance is very
important in these patient populations.
A 72-year-old gentleman who was diagnosed with CVID ten years earlier was referred to our
immunology clinic by his allergist for further evaluation and to help determine if immune globulin
replacement therapy was needed. On presentation, he had no complaints except for occasional fatigue
and nocturnal fevers. His physical exam was normal. Blood work showed mild leukocytosis with
neutrophils, lymphocytes and monocytes all increased. His previous laboratory results were reviewed
and were normal, other than extremely low IgG, IgM and IgA levels and mild eosinophilia that had no
explanation. He had stopped prior intravenous immunoglobulin therapy about eight years ago after his
“titers improved” and because of a rash. Given the high concern for malignancy in this population and
his unexplained fever, further studies were performed. He still had hypogammaglobulinemia. Flow
cytometry showed an aberrant CD4 positive T-cell population suggestive of a T-cell lymphoproliferative
disorder. Flow cytometry in 2004 was normal. He was referred to hematology/oncology for further
evaluation. A bone marrow biopsy confirmed the finding of an aberrant T-cell population similar to the
one detected in his blood but with no other evidence of lymphoma or bone marrow lymphocytosis. He
was advised to resume IVIG replacement therapy and follow up closely with the oncologist.
[Date]
Hypogammaglobulinemia does not always indicate a diagnosis of CVID. Clinical and laboratory criteria
have been defined for this condition. Further studies should always be carried out in these patients.
This case illustrates the importance of close monitoring in these patients for the possible later
development of a malignancy.
247
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Arya Lalithakumari, MBBS
Hyperkalemia : to treat or not to treat?
First Author: Arya Lalithakumari, MBBS second authors: Shyam Ganti MBBS, Vivek Variar MD
A 93 year old patient was admitted for dizziness from anemia. She had a history of mastocytosis and had
associated thrombocytosis for which she was on angrelide. Admission work up revealed potassium level
of 6.4 which prompted treatment with calcium gluconate, insulin and dextrose. However there were no
EKG changes of hyperkalemia. The kidney functions were normal and she was not on potassium
supplements. It was then noticed that her platelet count was 678,000. In presence of marked
thrombocytosis, a request was placed for measuring plasma potassium and serum potassium from a
freshly collected sample. This resulted in serum potassium of 5.9 with a plasma potassium of only 5, thus
proving an example of spuriously high potassium values.
[Date]
Pseudohyperkalemia is considered to be present when the plasma potassium differs from serum
potassium by more than 0.4 mmol/L. Pseudohyperkalemia has been described in the presence of
thrombocytosis. The pathology is considered to be in vitro release of potassium from activated platelets.
But patients are often misdiagnosed with hyperkalemia and are inappropriately treated with
medications and invasive measures including dialysis for persistently high serum potassium. The
recognition of normal potassium in the plasma prevented us from treating our patient for an incorrectly
high potassium value during the following admissions. The need to check a plasma potassium level
instead of a serum potassium level in thrombocytosis must be emphasized among clinicians not only
since it is of cost benefit from avoiding overtreatment and hospital admissions but also because it
prevents patient harm with inappropriate treatment of a normal potassium level.
248
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Andrea Landon, DO
Coexistent Xanthogranulomatous Pyelonephritis and Renal Cell Carcinoma
First Author: Andrea Landon, DO Andrea Landon, DO, Amir Koldor MSIII, Aaron Roberts, MD, Mark
Schauer, MD, FACP
Introduction: Xanthogranulomatous Pyelonephritis (XGP) is a rare inflammatory process in which renal
parenchyma is replaced by lipid-laden macrophages (xanthoma cells). It is frequently mistaken for renal
cell carcinoma (RCC) due to similarities in clinical presentation, laboratory results and radiological
findings. Confirmatory diagnosis is based on histopathological examination. We present an interesting
case of coexisting XGP and RCC.
Case Description: DS, a 73-year-old woman, presented with three months of worsening, sharp, leftsided flank pain radiating throughout her abdomen associated with anorexia, nausea, constipation, a 10
pound weight loss, night sweats and a new abdominal mass. Laboratory investigations showed
leukocytosis and hemoglobin of 5.5. Urinalysis results were +1 proteins, +2 ketones, +3 leukocyte
esterase, +1 hemoglobin, 48 RBCs, and >180 WBCs. CT abdomen/pelvis revealed several intraabdominal
abscesses, an obstructing staghorn calculi in the left kidney, and a heterogeneously enhancing mass in
the upper pole of the left kidney concerning for RCC. Multiple Jaxton-Pratt (JP) drains were placed and
empiric antibiotics were started. Abscess fluid cultures grew Proteus Mirabilis. One week later, she
underwent a left radical nephrectomy with an abdominal washout after no significant improvement
with medical management. She tolerated the surgery well and was discharged home a few days later.
Final pathology showed clear cell RCC and granulomatous pyelonephritis.
[Date]
Discussion: XGP is a form of chronic pyelonephritis associated with chronic urinary tract obstruction and
infection. It commonly presents diffusely, but focal infections are seen, as in this case. Patients are
typically middle-aged women presenting with fever, flank pain, weight loss and urinary tract symptoms.
The most common pathogens found on urine culture at diagnosis are E. coli and P. mirabilis. Most cases
involve a single kidney and treatment involves antibiotics in combination with a partial or total
nephrectomy. RCC, the seventh most common cancer in the United States, has a slight male
predominance and most patients present in the sixth or seventh decade of life. Risk factors are smoking,
obesity and hypertension. Prior to routine use of radiological imaging, patients typically presented with
a triad of hematuria, flank pain and a palpable abdominal mass. As imaging frequency has increased,
over half of all patients are now diagnosed incidentally. Prognosis is indirectly related to how early the
patient is diagnosed. To date, at least 10 case reports have shown coexisting XGP and RCC. Although it
remains unknown whether one predisposes to the other, it is important to consider their coexistence
and provide appropriate and timely treatment to ensure the best prognosis for the patient.
249
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Larry McMann, MD
Idiopathic Occipital Neuralgia a Rare Cause of Debilitating Headache
First Author: Larry McMann M.D., Tiba Alwardi M.D., Vesna Tegeltija M.D., Salwan Al-Mutar M.D., Reem
Al-Mahdawi M.D., Hussam Sabbagh M.D., Sarwan Kumar M.D., Khalid Zakaria M.D., Zain Kulairi M.D.
Introduction: Occipital neuralgia is usually defined as paroxysmal stabbing pain in the greater or lesser
occipital nerve distribution. Although there is no published data to suggest the incidence of occipital
neuralgia (ON), it is generally considered a very rare cause of headache.
Objective: We are reporting a case of occipital neuralgia. Learning objectives of this case are 1. Identify
the presentation of occipital neuralgia 2. Judicious use of diagnostic tools and treatment
Case: A 27-year-old female presented to the ER with episodes of severe intermittent headache over the
past 3 weeks. Prior to her presentation at admission she reported 2 episodes of intermittent pain on the
right occipital region. She promptly followed with her primary care physician who prescribed her oral
steroids. The two weeks following the initial episodes were symptom free.
On the day of admission she was watching television when she experienced a recurrence of the 10/10
right sided occipital headache with radiation over her vertex. Initial vital signs were unremarkable,
however, physical exam was significant for tenderness over the right occipital region of the scalp. Labs
were within normal limits. MRI did not reveal any abnormality. A consultation to neurology was
obtained and the patient was started on carbamazepine, gabapentin and narcotics, which provided little
relief. The patient’s distribution of pain in the greater occipital area in addition to ruling out secondary
causes of headache made ON the likely diagnosis. Pain management was consulted and greater
occipital nerve block was performed which provided complete resolution of her symptoms. She was
discharged home with carbamazepine the following morning and continued to be symptom free at
follow up.
Discussion: ON is a rare cause of headache that has no published data on incidence. Since this is a rare
disorder there is limited evidence in the literature to support the full understanding of its physiology and
treatment.
Currently, the diagnosis is made by history, characteristics described in the International Headache
Society, exclusion of referred pain by CT/MRI and anesthetic block of the occipital nerve. Patients with
severe symptoms can continue to have a debilitating headache despite conservative management. The
best treatment in the acute setting is the same intervention for diagnosis, which is an occipital nerve
block. Patients with recurrent ON symptoms despite steroid injections benefit from botulinium
injections and pulsed radiofrequency.
[Date]
Conclusion: This case illustrates the detailed diagnostic evaluation and the need for high suspicion by
the primary physicians to consider ON. It is often challenging to diagnose, yet it is critical to do so as
early diagnosis and treatment can maximize recovery.
250
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Larry McMann, MD
A Case of Cervical Manipulation Causing Stroke & Exploring its Biomechanics.
First Author: Larry McMann M.D.,Rudin Gjeka M.D., Dustin Reynolds, Firas Ido, Reem Al-Mahdawi M.D.,
Hussam Sabbagh M.D., Alaeddin Maeza M.D., Sarwan Kumar M.D., Zain Kulairi M.D.
Introduction: Manipulation of the cervical spine has been considered an effective treatment modality
by alternative healers, predominately chiropractors. The risk of having trauma to the vertebral-basilar
system resulting in a stroke is of major concern.
Objective: We present a case of vertebral artery dissection after cervical manipulation. Learning
objectives for this case are 1. Recognize characteristic clinical scenario for vertebral artery dissection
after cervical manipulation 2. Judicious prescribing habits for cervical manipulation
Case: A 43-year-old female presents to the emergency room with left sided upper and lower extremity
weakness after cervical manipulation. She had been having occipital headaches and neck discomfort
over the preceding 3 days. On the morning of admission she visited a chiropractor where they
performed cervical manipulation. Later that afternoon, while driving her vehicle she developed vertigo.
She then attempted to ambulate to her front door when she got profoundly weak and paralyzed on her
left side.
In the Emergency Department her blood pressure was 227/139, remainder of her vital signs were within
normal limits. On Physical exam she had hemiparesis on the left side of her body. Given her focal
neurological deficits a stroke was suspected, Computed Topography (CT) of the brain without contrast
was ordered and was unremarkable. Tissue plasminogen activator was administered in the emergency
room.
CT angiography was later performed to localize the lesion and it demonstrated a vertebral artery
dissection on the right side. It was decided that the patient would benefit from endovascular
intervention and was transferred to an institution in the local area for the procedure.
[Date]
Discussion: The internist should always be vigilant of possible vertebral artery dissection in a young
patient presenting with vertigo or weakness after cervical manipulation. Since this is a rare entity and
many practitioners are unaware of this complication, there can be oversight in obtaining a proper
history of cervical manipulation. Arterial dissection due to cervical manipulation is rare. Studies suggest
that 1 in 2,000,000 cervical manipulations results in a dissection in the verterbal-basilar system.
251
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Talin Nemri, MD
Catastrophic antiphospholipid syndrome following bariatric surgery!!
First Author: Talin Nemri, MD Rudin Gjeka, MD Kavyashri Kodlipet Jagadeesh, MD Jandark Yuseif, MD Zain
Kulairi, MD
Introduction: Catastrophic antiphospholipid syndrome (CAPS) is a rare but potentially life-threatening
condition characterized by diffuse vascular thrombosis, leading to multiple organ failure developing over a
short period of time in the presence of positive antiphospholipid antibodies (aPL).
We present a middle age female with CAPS who survived after treatment with anticoagulation plasma
therapy and intravenous corticosteroid
Case: A 56-year old female with history of antiphospholipid syndrome presented with severe weakness one
week after having a bariatric surgery. On evaluation her vital signs were significant for blood pressure of
150/90 mmHg and heart rate of 90 beat/minute. Systemic examination was noncontributory.
Initial laboratory results were significant for creatinine 1.4 mg/dl, platelets 99000/mm3 and Hemoglobin 9.8
mg/dl. In the next few days blood pressure start increasing to 200/110 mmHg, creatinine went up to 5 mg/dl,
platelets dropped to 55000/mm3 and hemoglobin dropped to 7.1mg/dl. Patient also developed severe
pleural effusion and non-sustained ventricular tachycardia. Kidney biopsy showed thrombotic
microangiopathy. Serological testing showed a high titer of anti-phospholipids, anticardiolipin antibody and
positive anti-ß2 glycoprotein-I antibody.
Based on the above findings, catastrophic antipohospholipid syndrome was diagnosed. Patient was started
on anticoagulation, plasma exchange, hemodialysis and glucocorticoids. In few days her platelets count,
hemoglobin as well as her shortness of breath improved. She was sent home on dialysis, after two months
kidney functions improved significantly and patient didn’t require dialysis anymore.
Discussion: CAPS a severe form of antiphospholipid syndrome, developing in about 1% of cases of classic
antiphospholipid syndrome was first described in 1992. Criteria for diagnosing CAPS include: (1) Evidence of
involvement of three or more organs, systems and/or tissues; (2) Development of manifestations
simultaneously in less than a week; (3) Confirmation of histopathology of small vessel occlusion in at least
one organ or tissue; (4) Laboratory comfirmation of the presence of antiphospholipid antibodies (Lupus
anticoagulant and anticardiolipin antibodies).
[Date]
Our patient met all the criteria for diagnosis since she had 3 organs involved (Kidney, Heart and bone
marrow), all developed in less than a week, with biopsy of the kidney showing thrombotic microangiopathy,
and she had positive antiphospholipid antibodies. We attribute her recent bariatric surgery as a precipitating
factor of her CAPS. Surgery is the second most common precipitating factor following infection. Other factors
include oral anticoagulation withdrawal/low INR, medications, obstetric complications, neoplasia, and SLE
flare. Treatment guidelines for CAPS include a combination of anticoagulants (AC), corticosteroids (CS),
intravenous immunoglobulins (IVIG), plasma exchange (PE), and cyclophosphamide. However, new
therapeutic modalities have emerged for the treatment of CAPS, especially in cases of refractory CAPS. These
treatment modalities include rituximab, defibrotide, and eculizumab.
252
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Otavio Pereira Rodrigues, MD
Epigastric pain in cirrhotic patient caused by primary gastrointestinal aspergillosis:
case report & literature review
Otavio Pereira-Rodrigues, MD; Estela Mogrovejo, MD; Norka Quillatupa, MD
Background: Primary gastrointestinal aspergillosis is extremely rare. Aspergillosis most frequently occurs
in the lungs or sinuses after inhalation of spores. However, conidia are not only inhaled but also
ingested, and isolated aspergillosis of the gastrointestinal tract has been described in few case reports.
The major risk factor for primary gastrointestinal involvement is an underlying severely
immunocompromised state such as long term corticosteroid use, transplantation, AIDS and
chemotherapeutic toxicity altering normal gastrointestinal immunity to allow Aspergillus entry by
disrupting mucosal barriers. Aspergillosis involving the digestive tract in immunocompetent patients has
rarely been reported.
Case: A 74-year-old male with alcoholic liver cirrhosis, portal hypertension, esophageal varices,
gastropathy, peptic ulcer disease and diabetes mellitus presented with a 3 day history of epigastric pain
and nausea. Physical examination showed epigastric tenderness. An EGD revealed a 1 cm non-bleeding
cratered ulcer in the duodenal bulb and a 3 cm non-bleeding cratered ulcer in the duodenal sweep.
Biopsies were taken. GMS stain revealed the presence of aspergillus invading the tissue and
immunohistochemical stain for Helicobacter pylori was negative. Computed tomography of the sinuses
and chest radiography were normal and HIV was negative. The patient was treated with oral
voriconazole for 6 weeks. An EGD control showed healed duodenal bulb and sweep ulcers. Control
biopsies were negative.
[Date]
Comment: Aspergillosis is almost exclusively considered a pulmonary disease with secondary
hematogenous dissemination in immunocompromised patients. However recent reports reveal
pulmonary aspergillosis in immunocompetent patients, describing associations with other conditions as
influenza, pneumonia, COPD, sepsis, liver failure, diabetes, alcoholism, chronic granulomatous disease
and surgery. In this setting, the reported patient had primary gastrointestinal aspergillosis, was not
immunocompromised but had a history of diabetes and alcohol intake which might have played an
important role in the development of duodenal aspergillosis.
253
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Suraj R Raheja, MD
Acute Thrombocytopenia from Severe Hepatitis C Viremia
First Author: Dr. Suraj Raheja Second Author: Dr. Malathy Kilaru Senior Staff: Dr. Sheela Tejwani
Chronic or untreated Hepatitis C infection may cause thrombocytopenia through a number of
mechanisms. These include hyper-splenism from portal hypertension, decreased liver thrombopoietin
production, or bone marrow suppression from the virus itself. Historically, the severity of
thrombocytopenia increased in parallel with the development of extensive fibrosis or cirrhosis. Here we
present a case showcasing the simple degree of viremia to be primarily responsible for acute changes in
platelet counts.
Our patient is a 47 year old female with Hepatitis C that was diagnosed 14 years ago. She was initially
treated with peg-interferon mono-therapy. Though she responded well, insurance issues precluded her
from further therapy after only 6 months. She was then seen to have pancytopenia, with platelets
ranging from 50-100 K/uL, and hemoglobin ranging from 6 to 10 g/dL.
She later developed end-stage renal disease from membrano-proliferative glomerulonephritis. As part
of a renal transplant workup two years ago, the liver was evaluated by imaging and there was no
evidence of cirrhosis. Liver biopsies were also performed, showing only minimal peri-portal fibrosis. In
addition, her Hepatitis C viral load at that time recorded as 313,000 IU/mL. In the absence of cirrhosis,
Gastroenterology was unable to explain her thrombocytopenia.
Now, two years later, the patient awoke to find gingival bleeding and mild vaginal bleeding. Labs found
an acute drop in platelets to just 6 K/uL (from 84 K/uL two months prior). The etiology of the drop was
not immediately clear. It was noted that the patient’s hepatitis C viral load now measured greater than
69,000,000 IU/mL. Immediate treatment for this was delayed because of the severe cytopenias. With
transfusions, her hemoglobin stabilized. Her platelet counts, however, could not be sustained despite
multiple transfusions. Bone marrow biopsy was pursued, which found hypo-cellular marrow with
diminished tri-lineage hematopoiesis. There was no evidence of myelodysplasia, acute leukemia, or
plasma cell neoplasm. Anti-phospholipid syndrome work-up was also negative.
The patient was started on steroids, and had some improvement in her platelet count to 50 K/uL. She
was discharged with close follow up with Hepatology, who decided to start sofosbuvir and simeprevir
for treatment of her viremia. After five weeks of therapy, the patient’s hepatitis C viral count improved
to less than 43 IU/mL. Simultaneously, her platelet count improved to 121 K/uL, and anemia improved
as well.
[Date]
The management of thrombocytopenia attributed to hepatitis C viral load is evolving as newer agents
become available for use. Though used historically, interferon may worsen platelet counts if used to
address Hepatitis C viremia. Though our case illustrates the complexity of acutely managing
thrombocytopenia due to high Hepatitis C viral loads, it also highlights the ability of such cases to quickly
respond to treatment. We submit this case as an outline for future encounters.
254
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Tarun Sharma, MD
UFO: Unidentified Foreign Object Causing Retroperitoneal Abscess
First Author: Tarun Sharma Second Author: Joel T. Fishbain MD, FACP
Background: Foreign body ingestion may be an underreported event with gastrointestinal perforation
being a very uncommon occurrence (estimated ~1%). Acute abdominal symptoms may develop and the
object is typically identified at the time of surgery. Severe abdominal pain and/or presence of an abscess
generally requires surgical intervention.
Case report: A 62 year old Vietnamese male with past medical history of hypertension and gout
presented with a 2-3 day history of acute severe midepigastric abdominal pain radiating to his back. He
was afebrile with a normal examination except for significant midepigrastic tenderness to palpation,
guarding and fullness. His admission white blood count was 23,000. A CT scan of the abdomen revealed
9.9 x 4.9 x 6.5 cm fluid collection inferior to the pancreas and in the retroperitoneal space (mesenteric
root). A non-metallic 3 cm linear foreign body was seen within the abscess cavity and exterior to the
small bowel lumen. A CT guided drain was placed and E. coli grew from cultures. The patient had
marked improvement and was discharged on oral antibiotic therapy.
[Date]
Discussion: Foreign body ingestion normally results in no symptoms with eventual passage of the object.
The peak incidence of such ingestions is 6 months to 6 years age. In adults, presence of dentures is the
most common risk factor for foreign body ingestion. Sharp objects such as chicken bones and fish bones
rarely result in perforation with subsequent abscess formation. Though surgical intervention is typically
performed for object removal, non-operative conservative management can be undertaken for patients
with minimal symptoms of peritonitis. A conservative approach was taken with our patient due to
object’s location and surrounding inflammatory process, increasing his surgical risk. The patient
responded to antibiotic therapy after CT guided drainage. Repeat CT 1 month later showed more linear
densities as the patient’s diet had remained unchanged. This case exemplifies medical management of
foreign body GI tract perforation.
255
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Travis Tagami, DO
Acute Aortic Regurgitation in a Dialysis Patient
First Author: Travis Tagami Second Author: Rami Khoury Abdulla Third Author: Nicole Marijanovich
Despite advances and widespread availability of medical technology, a good history and physical
examination remain the cornerstone of a comprehensive medical evaluation. We are presenting a case
where examination skills were able to make the diagnosis and guide further diagnostic and therapeutic
interventions.
A 45 year old male with a history of dialysis-dependent end stage renal disease presented to the
emergency room with chest pain and associated shortness of breath. He described a pressure-like,
retrosternal chest pain that was worse with exertion and progressing over the last two weeks.
Echocardiography three months prior to admission showed left ventricular wall thickening and dilated
atria with no other abnormalities. Upon physical exam on current admission his vital signs were stable.
He was noted to have scattered crackles at the bases of his lungs and a new diastolic murmur. A chest xray showed mild pulmonary edema and he was found to have an elevated troponin with no ischemic
changes on EKG. A cardiac ultrasound was performed which showed severe aortic regurgitation with a
3.1 x 1.2 cm mass attached to the left coronary leaflet moving in and out of the left ventricle. He was
immediately taken for surgery where the vegetation was removed and a mechanical aortic valve was
inserted. Tissue cultures were obtained and a diagnosis of culture negative endocarditis was made. He
recovered well from surgery and he was discharged from the hospital with a four week course of
antibiotics. At two week follow up, there was remarkable improvement in his symptoms.
[Date]
This case illustrates the importance of early recognition of aortic regurgitation. Without close attention
to physical exam findings of a new murmur and subsequent evaluation with echocardiogram, this
diagnosis could easily have been missed or delayed leading to severe complications.
256
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Sunit Y Tolia, DO
An Unusual Presentation of Malignant Melanoma
First Author: Sunit Y Tolia, DO Lyle Goldman M.D., Farooq Minhas M.D., Irina Shanidze M.D.
Introduction: Melanoma, a type of skin cancer that originates from uncontrolled growth of pigment cells
called melanocytes. It is known to metastasize to skin, brain, lung and rarely to the ovaries. It is the fifth
most common cancer in men and seventh in women. Up to 90% of melanomas are cutaneous in origin
and are called melanoma of known primary (MKP); however, those discovered secondary to metastasis
to lymph nodes or visceral organs without any primary site are called melanoma of unknown primary
(MUP).
Case Description: A 38-year-old premenopausal woman presents with a chief complaint of “abdominal
bloating and lumbar pain.” Initial abdominal and chest x-ray showed stool within the colon and a 4-cm
mass in the right lower lobe respectively. Subsequently a computer tomography (CT) of the chest,
abdomen, and pelvis was done and it re-confirmed the pulmonary mass, presence of liver lesions, large
amount of ascitic fluid as well as left pelvic mass likely to be ovarian in nature. Paracentesis and CTguided biopsy of the lung were performed. Ascitic fluid was negative for malignant cells; however, the
lung biopsy showed the presence of metastatic undifferentiated carcinoma of indeterminate origin. In
addition to the biopsy, CA-125 levels were elevated to 1,036 units/mL and thus the working diagnosis
was ovarian cancer. Upon gynecological evaluation, the patient underwent exploratory laparotomy,
modified radical hysterectomy with bilateral salpingo-oophorectomy and tumor debulking surgery. Postoperative recovery was uneventful. Moreover, pathology of surgical specimen revealed presence of
metastatic melanoma involving bilateral ovarian surfaces, peri-adnexal soft tissue, tubal and uterine
serosa, pelvic peritoneum, lesser omentum, peripancreatic and adipose tissue. In addition, right lung
and right neck lymph node excision was also positive for metastatic melanoma.
Furthermore, magnetic resonance imaging (MRI) of the brain was performed which showed numerous
metastatic lesions; the largest one present in the right parietal region. Genetic analysis identified
alterations in BRAF V600E gene and TERT promoter region, as a result was treated with Dabrafenib.
Patient responded well to both the chemotherapy and whole brain radiation. The patient is still alive
and improving clinically.
[Date]
Conclusions: Metastasis of malignant melanoma to the ovaries can mimic a primary ovarian cancer, like
in our case, thus posing a diagnostic challenge. Ovarian involvement by metastatic malignant melanoma
is relatively rare and only 77 cases are reported in literature, this being the 78th case. Moreover, this is
the first reported case of melanoma of unknown primary that presented with metastatic lesions to both
visceral organs and lymph nodes.
257
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Shrey Velani, MBBS
Neuromyelitis Optica mimicking stroke
First Author: Shrey Velani, MBBS Second Author: Yash Agrawal, MBBS Third Author: Bhavik Khajuria, DO
Fourth Author: Amir Koldorf, DO
Introduction Neuromyelitis optica (NMO or Devic disease) is an inflammatory disease of central
nervous system in the spectrum of demyelinating diseases like multiple sclerosis (MS) characterized by
bilateral optic neuropathy and cervical myelopathy. Traditionally considered a variant of multiple
sclerosis, NMO is now recognized as a distinct clinical entity based on unique immunologic features. The
discovery of a disease-specific serum NMO-IgG antibody that selectively binds aquaporin-4 (AQP4) has
led to increased understanding of a diverse spectrum of disorders.
Case Description We describe a 61 year old right handed woman who presented with progressive right
sided weakness over 2 days. She had remote history of legal blindness of unknown etiology and was
never worked up in past. Initial exam revealed light perception without movement perception, fixed
pupils, and optic disc pallor extending beyond the disc, decreased right arm and right leg strength (3/5).
CBC, CMP, CRP, ANA, PPD, Troponins, EKG, bilateral carotid duplex ultrasound and MRI brain without
contrast were unremarkable. MRI cervical and thoracic spine without contrast showed patchy
enhancement and expanded spinal cord from C1-C2 through C7-T1 and patchy enhancement at T9-T10.
Lumbar puncture showed clear, colorless CSF with high glucose, protein, IgG-2 oligoclonal bands and
later a positive NMO/AQP4-IgG. Patient met diagnostic criteria for NMO with optic neuritis, cervical
neuropathy extending through at least 3 vertebral segments on MRI and MRI brain without changes for
MS. She was started on solumedrol 1gm q24 for 5 days which improved her weakness symptoms. She
was transitioned to PO prednisone and azathioprine for 4-6 months with outpatient neurology follow
up.
[Date]
Discussion NMO is rare disease and early diagnosis very crucial for timely management and to prevent
catastrophic complications. Internists should have index of suspicion for NMO in appropriate clinical
settings. Acute attacks and relapses of NMO are generally treated with intravenous glucocorticoids
followed soon by plasmapheresis for refractory or progressive symptoms. For prevention of recurrent
attacks, treatment with systemic immunosuppression is the mainstay. However, there are no controlled
trials evaluating the treatment of NMO, and recommendations are primarily supported by data from
observational studies and by the clinical experience of experts. Mortality rates are high in NMO, most
frequently secondary to neurogenic respiratory failure, which occurs with extension of cervical lesions
into the brainstem or from primary brainstem lesions
258
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Andrew Whipple, DO
Severe Cholestatic Jaundice from an Unanticipated Diagnosis
First Author: Andrew Whipple, D.O., Timothy Schubert, D.O., Steve Abshagen, P.A.-C
Introduction: Primary (AL) amyloidosis is characterized by abnormal immunoglobulin light chains with
subsequent organ deposition and dysfunction. Up to 70% of systemic amyloid cases demonstrate
hepatic involvement, and typical findings include hepatomegaly and elevated alkaline phosphatase.
However, severe intrahepatic cholestasis with clinical jaundice is a rare finding seen in less than 5% of
cases, and carries a particularly poor prognosis. We present a patient with painless jaundice from severe
intrahepatic cholestasis who was found to have AL amyloidosis.
Case Description: A 72 year old female presented with a 2 month history of progressive pruritis,
jaundice, and diarrhea. She also admitted to fatigue and a 30 pound weight loss over the preceding 6
months but otherwise denied abdominal pain, melena, or alcohol use. Initial labs were remarkable for
total bilirubin 11.3 mg/dl, alkaline phosphatase 479 U/L, and liver enzymes twice the upper limit of
normal. Ultrasound demonstrated increased echogenicity of the liver, a 1.3 centimeter sludgeball in the
gallbladder, and no biliary dilatation. Hepatobiliary scan and endoscopic ultrasound were both
unremarkable. Liver biopsy subsequently revealed amyloidosis with amorphous, eosinophilic deposits
predominately within the portal areas, surrounding and compressing the bile ducts and intra-hepatic
blood vessels. Further laboratory workup resulted in a final diagnosis of AL amyloidosis.
[Date]
Discussion: Hepatic involvement in AL amyloidosis is common, however overall clinical manifestations
from this are mild or often absent. In two published series of primary AL-type amyloidosis, Kyle et al
reported the incidence of elevated serum total bilirubin levels (greater than 2 times upper limit of
normal) were between 4 and 8%. Cholestatic jaundice is infrequent and considered to be a pre-terminal
sign of hepatic amyloidosis. In fact, analysis by Gertz et al suggested an elevated total bilirubin > 3mg/dl
correlated with an average 1.8 month life expectancy, and 80% of reported patients died within 6
months after the onset of clinical jaundice. Physiologic cholestasis is related to direct compression of
intrahepatic bile ducts by amyloid deposits in the portal area and sinusoidal space. A low threshold for
liver biopsy at the onset of suspicion for amyloidosis can provide early diagnosis so that aggressive
treatment, or appropriate palliative options can be offered. Our patient serves as a reminder of the
variable presentations of amyloidosis and that it should be considered in the differential diagnosis of
severe intrahepatic cholestasis.
259
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Andrew Whipple, DO
Expanding the Differential Diagnosis for Painless Jaundice
First Author: Andrew Whipple, D.O., Christopher Begley, D.O., Akshay Amaraneni, M.D.
Introduction: Bouveret’s syndrome refers to gastroduodenal obstruction from gallstone impaction
which occurs in the setting of a cholecystoduodenal fistula. Depending upon the exact location and size
of the gallstone, a variety of clinical manifestations are possible. We describe a case of Bouveret’s
syndrome with the unique presenting symptom of painless jaundice.
Case Description: A 62 year-old female presented with a 3 week history of increasing jaundice, fatigue,
and nausea with an associated 15 pound weight loss. The patient denied abdominal pain and abdominal
examination was unremarkable. Initial laboratory studies were significant for total bilirubin 9.3 mg/dl,
alkaline phosphatase 477 U/L, aspartate aminotransferase 95 U/L, and alanine aminotransferase 111
U/L. Initial ultrasound revealed intrahepatic and extrahepatic biliary dilatation. Magnetic resonance
cholangiopancreatography (MRCP) showed a suspected calculus located in the proximal portion of the
duodenum with surrounding soft tissue thickening. Endoscopic gastroduodenoscopy (EGD) confirmed a
large gallstone in the duodenal bulb which occupied the entire lumen and partially protruded through
the pylorus. As this was unable to be removed endoscopically, the patient underwent gastrotomy and
removal of a 3.3cm gallstone. No fistulous tract was appreciated intraoperatively and is considered to
have closed spontaneously. Subsequently, the patient was treated supportively and discharged home on
post-operative day 7 with resolution of her symptoms and normalization of her laboratory values.
[Date]
Discussion: Bouveret’s syndrome was first reported in 1896 and remains an uncommon variant of
gallstone ileus, for which it comprises only 1-3% of cases. While a wide variety of presenting symptoms
have been reported, to our knowledge no case of Bouveret’s syndrome has presented as painless
jaundice, which in this case was a result of external CBD compression. The largest review was published
in 2006 by Cappell and Davis where they describe 128 cases. The most common presenting symptoms
were nausea, vomiting, abdominal pain, hematemesis, and weight loss. Less commonly, patients
reported an absence of abdominal pain in 29% and Jaundice in less than 2% of cases. The mean age of
patients at diagnosis was 74, and had a female predominance of nearly a 2:1 ratio. As in our case, EGD
reveals gastric outlet obstruction in almost all cases; however the source of obstructive process can be
identified only 69% of the time. While EGD is useful diagnostically, endoscopic gallstone retrieval is
usually not possible due to the size of the gallstone. Thus, treatment of the obstructive process most
often requires gastrotomy or enterolithotomy and is 90% successful.
260
MICHIGAN POSTER FINALIST - CLINICAL VIGNETTE Juraj Zahatnansky, MD
Peripheral neuropathy as a manifestation of Kikuchi-Fujimoto disease, a rare
presentation of a rare disease.
First Author: Juraj Zahatnansky, MD Christina Lang, MD Karthik Kannegolla, MD Rakshita Chandrashekar,
MD Richard Roach, MD
Case description: We present the case of a 30-year-old man with chief complaints of numbness and a
progressively worsening burning sensation in his extremities over the course of one month. His other
symptoms included polydipsia, vomiting, chills, and weight loss. Physical examination revealed no
cervical lymphadenopathy, but profound paraesthesia of hands and feet. With the patient’s smoking
history and diagnosis of SIADH per initial labs, a CT of his chest was performed to look for possible lung
malignancy. The study revealed left axillary lymphadenopathy that ultimately led to diagnosis of KikuchiFujimoto disease following an excisional biopsy of one of the lymph nodes.
The patient also underwent extensive evaluation for possible infectious and rheumatologic causes of his
symptoms, all of which were unrevealing. Cerebrospinal fluid analysis, bone marrow and skin biopsies
were all normal. Neurological evaluation, including MRI of the head and spine, was also negative except
for EMG, indicative of mild bilateral demyelinating sensorimotor polyneuropathy of the lower
extremities. A lower extremity angiogram did not show signs of vasculitis/narrowing and a toxicology
screen was also negative.
[Date]
Discussion: Kikuchi-Fujimoto disease or Kikuchi histiocytic necrotizing lymphadenitis is a benign, selflimited disease of unknown etiology that commonly presents with cervical lymphadenopathy and fever
in younger women. Neurological symptoms including peripheral neuropathy have been reported in the
literature, but are a rare presentation of this rare disease. This is what prompted continuation of the
patient’s work-up even after the diagnosis was made with the biopsy. It is the purpose of this case
report to add to the body of evidence and by it raise awareness of peripheral neuropathy as one of the
possible presenting symptoms of Kikuchi-Fujimoto disease. To our knowledge, there are no reports of
SIADH being associated with the disease, which would certainly make this case a unique one. However,
the patient was started on carbamazepine for neuropathic pain two weeks prior to being admitted to
the hospital. Since there are reports of carbamazepine causing SIADH, this is a more likely explanation.
Serendipitously, it was the SIADH which helped to make the diagnosis.
261
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Ashley M. Egan, MD
A Recurrent Broken Heart
First Author: Ashley M. Egan, MD Bradley W. Anderson, MD Arya B. Mohabbat, MD
Stress-induced cardiomyopathy, also referred to as Broken Heart Syndrome, is a relatively rare condition
affecting approximately 1-2% of patients presenting with acute coronary syndrome. It is almost
exclusively seen in postmenopausal women with documented low recurrence rates.
A 91-year-old Cambodian woman with a medical history significant for cholangitis with subsequent
ampulla of Vater sphincterotomy and cholecystectomy presented to the emergency department with
generalized weakness, abdominal pain, and fever. A preliminary diagnosis of cholangitis was made and
she was initiated on antibiotics. An endoscopic retrograde cholangiopancreatography (ERCP) revealed
choledocholithiasis and focal non-obstructing stenosis of the right main hepatic duct. She underwent
successful stone removal and dilation of the stenosis without procedural complication. Over the
following day, her abdominal pain and hyperbilirubinemia persisted. Physical examination revealed a
new cardiac murmur; transthoracic echocardiogram demonstrated an ejection fraction of 74% without
appreciable regional wall abnormalities. Continuing symptoms prompted repeat ERCP with stenting of
the right hepatic duct stenosis. Initially, the patient demonstrated clinical improvement but the
following day she developed chest pain and shortness of breath. An electrocardiogram showed ST
changes and serum troponin was mildly elevated raising concern for possible ischemia. Repeat
transthoracic echocardiogram, just two days after the first echocardiogram, demonstrated left
ventricular enlargement with an ejection fraction of 36% and new regional wall motion abnormalities.
The patient was transferred to the intensive care unit for further care. Severe coronary artery
atherosclerosis was noted on angiography, but coronary perfusion was judged to be TIMI grade III
indicating full perfusion; this led to the diagnosis of stress-induced cardiomyopathy. Interestingly, upon
further chart review, the patient developed stress-induced cardiomyopathy approximately six years
prior following previous ERCP. At that time, her left ventricular ejection fraction decreased to 35% but
subsequently improved to 65% within one month. Unfortunately, during her current hospital stay, the
patient died secondary to cardiogenic and septic shock.
[Date]
This case highlights the importance of further evaluation of suspected acute coronary syndrome to
delineate between myocardial infarction and other possible diagnoses. Up to 10% of patients with a
history of stress-induced cardiomyopathy can experience a recurrence, though this generally occurs
within the ensuing four years. Furthermore, the identification of Broken Heart Syndrome is crucial as the
treatment can potentially differ from standard care for myocardial ischemia since the condition is
thought to be a result of catecholamine excess. Ultimately, treatment of the underlying cause is key to
managing this transient disorder.
262
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Stanislav Henkin, MD
Got milk? High fat dairy diet causing severe reversible elevation of LDL-C
First Author: Stanislav Henkin, MD, MPH Second Author: Andrew Calvin, MD, MPH Third Author: Ananda
Basu, MD, FRCP
Introduction: Coronary artery disease is one of the leading causes of morbidity and mortality in the
United States. New lipid guidelines suggest initiating high-intensity statin for individuals with LDL > 190
mg/dL for primary prevention of coronary artery disease.
Case Discussion: A 59 year-old woman with a history of hypertension and hyperglycemia presented to
the Endocrinology Clinic for further evaluation of diabetes mellitus in the setting of fatigue and weight
loss. The patient was previously diagnosed with “mild diabetes” at the age of 8 and advised to avoid
carbohydrates. She started on metformin 4 months prior to presentation. On review of symptoms, she
reported 30 pound weight loss in the past 6 months. In order to regain weight while avoiding
hyperglycemia, the patient had been following a high-fat low-carbohydrate dairy diet. Family history
was positive for early-onset diabetes mellitus in several first degree relatives. Physical examination was
unremarkable. Laboratory evaluation was significant for hemoglobin A1c 6.3%, fasting glucose 110
mg/dL, C-peptide 0.9 ng/mL (normal for prevailing glucose concentrations), total cholesterol 379,
triglycerides 60, HDL-C 85 mg/dL, and LDL-C 282 mg/dL. Genetic testing was positive for missense defect
in the glucokinase gene, consistent with maturity onset diabetes in the young, type 2. The patient was
seen by a dietician, who suggested that she switch from a high-fat dairy diet to unsaturated food
sources and increase her caloric intake to 1800-2000 calories per day. After incorporating these changes
for 3 months, the patient’s LDL-C decreased to 109 mg/dL, she was able to regain several pounds with
symptomatic improvement of fatigue, and her metformin was discontinued.
Discussion: Maturity onset diabetes in the young (MODY) is a heterogenous disorder characterized by
non-insulin dependent diabetes most commonly caused by impaired glucose sensing by the b cells
resulting in a shift of glucose-insulin coupling to the right. This results in a higher than normal glucose
threshold required for initiation of insulin secretion. Consequently, patients develop mild
hyperglycemia, often controllable with diet alone, and not associated with vascular complications.
[Date]
In an attempt to control the mild hyperglycemia, this patient strictly avoided carbohydrates while
consuming excess saturated fat with resultant severe dyslipidemia. While The American College of
Cardiology/American Heart Association (ACC/AHA) guidelines would suggest that a patient with an LDLC >190 mg/dL be initiated on high-intensity stain, modest dietary intervention in this patient was
extremely efficacious with a reduction in LDL-C of >50% and also helpful in managing her
MODY. Research suggests that lowering intake of saturated fats from 14-15% to 5-6% of total calories
can lower LDL by 11-13 mg/dL (~11%). This case underlies the importance of detailed dietary history as
part of a complete cardiovascular evaluation.
263
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Thanh Phan Ho, MD
Renal colic unveiling underlying lymphoma
First Author: Thanh Phan Ho, MD Syed Ahsan Rizvi, MD
Introduction: Renal stones are increasing in the general population, and this has been partly attributed to
changes in diet and body size. In rarer instances, renal stones are precipitated by hypercalcemia
secondary to underlying illness. In the ambulatory population, hyperparathyroidism is the most common
etiology of hypercalcemia. In the hospital setting, however, hypercalcemia is most commonly observed
as the result of malignancy.
Case Description: 21-year-old male with unremarkable medical history presented with sudden onset left
lower quadrant pain to local student health clinic and subsequently transferred to our institution for
hospital admission. No other associated symptoms or constitutional symptoms such as fever, chills, or
weight loss. Patient was afebrile and hemodynamically stable; his physical exam was unremarkable and
without palpable lymphadenopathy. Laboratory results were notable for hemoglobin 9.5, MCV 87.0,
potassium 3.5, calcium 13.0, creatinine 2.8, BUN 31, uric acid 9.1; additional work up including LDH,
HCG, AFP, TSH were within normal limits. CT abdomen/pelvis showed massive lymphadenopathy
throughout the chest, abdomen and pelvis; 1.2 cm partially calcified pulmonary nodule in the right
middle lobe; 4 mm renal stone in the left ureterovesical junction resulting in obstruction of the left
ureter and moderate pyelocaliectasis. Patient passed renal stone during hospital course uneventfully,
with resolution of pain. Stone analysis revealed 90% calcium phosphate and 10% calcium carbonate. He
was started on allopurinol for tumor lysis syndrome prophylaxis, with reduction of uric acid level to
normal limits. Patient’s hypercalcemia responded to normal saline and calcitonin; his creatinine
improved as well. His normocytic anemia remained stable. Patient underwent mediastinoscopy with
lymph node biopsy which demonstrated B-cell lymphoma, unclassifiable, with features intermediate
between diffuse large B-cell lymphoma and Hodgkin lymphoma. He was discharged, to follow up with
Hematology clinic for further management.
Discussion: This case presents a new diagnosis of lymphoma in an otherwise healthy young individual
[Date]
without B symptoms or remarkable physical exam findings who presented with renal colic. The patient
had a calcium stone, consistent with his hypercalcemia which responded to fluid hydration and
calcitonin. Hypercalcemia is seen with both Hodgkin and non-Hodgkin lymphoma. Lymphoma-associated
hypercalcemia is most often mediated by the vitamin D pathway involving dysregulated calcitriol
production and increased intestinal calcium absorption, though humoral hypercalcemia of malignancy
mediated by parathyroid hormone-related protein may also play a role. While data regarding the
clinical impact of hypercalcemia in lymphoma is scarce, patients with hypercalcemia of malignancy are
usually symptomatic. Renal colic, specifically, is an unusual clinical presentation at diagnosis of
lymphoma. But as we show here, it is a symptom which warrants the attention of clinicians for further
investigation of potential underlying malignancy.
264
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Gregory P Kaufman, MD
Renal failure and nephromegaly manifesting from progressive CLL
First Author: Gregory P. Kaufman, MD James R. Gregoire MD, Mariam P. Alexander MD, LaTonya J. Hickson
MD
Learning Objectives
1.
2.
3.
Recognize the differential diagnosis for renal failure in the CLL population, always exclude
obstruction
Know the common processes resulting in nephromegaly
Understand CLL renal invasion is common, but not frequently associated with renal failure
Case Description: A 74-year-old woman with a history of CLL under observation presented to the outpatient
clinic with three months of progressive functional decline. Examination revealed an ill appearing patient with
normal vital signs, and stable axillary adenopathy. Laboratory evaluation showed a white blood cell count of
30 k/uL with an absolute lymphocyte count of 24 k/uL (increased from of 8 k/uL three months prior). Other
laboratory studies revealed a creatinine of 5.6 (increased from 1.4 three months prior), BUN of 98,
bicarbonate of 19, and a potassium of 4.6. She was admitted to the hospital for further evaluation.
A CT abdomen showed no evidence of hydronephrosis, but did reveal a 50% increase in kidney size compared
to a previous study from 5 years prior. A urinalysis showed 10 RBC/hpf of which >25% were dysmorphic and a
predicted 24 hour protein of 2.5 grams. Despite intravenous hydration she remained oliguric without
improvement in her serum creatinine. Given suspicion for a glomerular process she underwent a renal biopsy
and was started on empiric steroids. The biopsy revealed diffuse infiltration of the interstitial parenchyma by
neoplastic small lymphoid cells without evidence of vasculitis. Electron microscopy revealed preserved
podocyte foot processes and no thickening or focal deposition along the basement membrane.
The patient improved with steroids and initiated immunochemotherapy appropriate for her renal function
under the guise of her hematologist for progressive CLL. Following three cycles her creatinine has stabilized
at 1.7.
Discussion: The differential diagnosis of renal failure in the CLL patient population is broad encompassing a
higher frequency of extrarenal obstruction due to pelvic lymphadenopathy as well as intrinsic causes
including membranous nephropathy, minimal change disease (higher in T cell CLL), type 1 cryoglobulinemia,
and less commonly leukemic infiltration of the renal parenchyma. This case illustrates the importance of
incorporating careful review of imaging studies into the clinical context of a patient’s presentation. Bilateral
nephromegaly in an adult can be seen in polycystic kidney disease, distal obstruction, early diabetes mellitus,
sarcoidosis, rare hereditary disorders such as Von Hippel-Lindau and nephroblastomatosis, as well as
infiltrative disorders such as IgG4 disease or lymphoma/leukemias.
[Date]
Renal infiltration in CLL is highly prevalent in autopsy studies (60-90%), but uncommonly associated with
renal dysfunction. Immunochemotherapy such as anti-CD20 agents and non-renally eliminated drugs such as
chlorambucil have anti-leukemic efficacy and can reverse renal dysfunction when attributed to CLL
parenchymal infiltration.
265
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Hannah C Nordhues, MD
Moans without Stones: A Case of Spontaneous Renal Artery Dissection
First Author: Hannah C Nordhues, MD
Spontaneous renal artery dissection (SRAD) is a rare entity, which has a prevalence of 0.036—0.05% of
dissections in large angiographic studies. It is most commonly associated with underlying vascular or
connective tissue disorders such as Fibromuscular Dysplasia, Marfan’s Syndrome, or Ehlers-Danlos.
Other associations include malignant hypertension and severe physical exertion. Its clinical
manifestations range from asymptomatic renal infarction to severe abdominal pain, nausea, headache,
hematuria, and hypertension.
We present a case of a previously healthy 41 year old male who presented to his local emergency
department with five hours of constant right-sided abdominal and flank pain with associated nausea. He
was evaluated for presumed cholelithiasis and nephrolithiasis with unremarkable initial studies. He was
dismissed with pain medication and instructions for outpatient abdominal ultrasound. The following
morning his abdominal ultrasound was normal. He re-presented to the ED where a CT scan with IV
contrast revealed a wedge shaped infarct of the right kidney. His pain continued to progress requiring
transfer to another facility for further management.
During transport to our facility he became hypertensive to 171/101 mmHg. His creatinine remained
stable at 1.0 and he was initiated on Lisinopril 5 mg daily. CT angiogram revealed a thrombosed
dissection in a second order branch of the right renal artery. In the setting of the acute thrombosis,
imaging could not rule out fibromuscular dysplasia.
No surgical intervention was undertaken and after 24 hours he was transitioned from Heparin to
Clopidogrel. His pain improved, his renal function remained stable, and his blood pressure was well
controlled. His treatment consisted of Clopidogrel 75 mg daily for three months, and then Aspirin 325
mg daily for 1 year following his event.
Due to concern for possible fibromuscular dysplasia as an underling etiology for renal artery dissection,
a carotid artery ultrasound was performed and was normal. His CT angiogram at 6 weeks showed
interval improvement of the thrombus and infarction with only minimal renal scarring and partial
recanalization of the artery. Although fibromuscular dysplasia statistically is the most likely cause of
spontaneous renal artery dissection, all other visualized vessels in the abdomen appear unaffected. At
the six week follow-up, his hypertension had completely resolved and no longer requires medical
management.
[Date]
Although SRAD is considered extremely rare, one study reported 35 symptomatic cases over 40 years at
a single institution. SRAD has a wide variety of clinical presentations. Asymptomatic, or mild, selfresolving SRAD may lead to an underestimate of this condition’s true prevalence. Prognosis is good with
appropriate intervention, however early recognition remains key. In atypical cases of abdominal and
flank pain, SRAD should be considered in the differential diagnosis.
266
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Kelly M Pennington, MD
Lupus There It Is: Atypical Presentation of Lupus in the Setting of Concomitant
Plasmodium Infection
First Author: Kelly M Pennington, MD Christine Tran Ruth Bates, MD Prashant Sharma, MD, FACP
Introduction: Several case-series have shown that systemic infections can lead to earlier presentation
or recognition of systemic lupus erythrematosus (SLE). In these circumstances, patients can present
with non-specific signs and symptoms, making diagnosis challenging. Here, we present a previously
healthy patient whose first presentation of nephrotic syndrome was in the setting of concomitant
Plasmodium infection.
Case Presentation: A previously healthy 18 year-old female presented to the emergency department
with a two-month history of chronic nausea, dysphagia, and a 40-pound weight loss. Ten-weeks prior to
admission, the patient had a month long visit to India; she did not receive immunizations or antiparasite prophylaxis. While in India, she developed nightly fevers with nausea and vomiting and was
symptomatically treated at a local hospital with unknown medications. Her fevers resolved; however,
she remained chronically nauseated with episodic non-bloody, non-biliary emesis.
Physical examination showed an afebrile African female with diffuse abdominal tenderness without
rebound or splenomegaly. No edema, joint tenderness/erythema or skin rashes were appreciated.
Other systemic examination was normal.
Laboratory studies were positive for microcytic anemia, elevated creatinine with nephrotic range
proteinuria, hematuria with dysmorphic red blood cells, and pyuria. Initial work-up for infectious,
autoimmune, and malignant causes were negative except a weakly positive ANA, weak cold and warm
agglutinins, and low C3/C4. Anti-dsDNA and anti-phospholipid antibodies were negative. Initial
peripheral blood smears were non-revealing. On the third malaria smear, a few Plasmodium species
were identified, however not enough to speciate accurately. Despite aggressive IV hydration, her
creatinine remained elevated. A renal biopsy revealed crescentic and necrotizing lesions with focal
mesangial hyper-cellularity. Immunofluorescence studies demonstrated global granular capillary loop
reactivity and tubular basement membrane deposits with interstitial immunoglobulin deposits. These
histologic findings were consistent with lupus nephritis. She was started on high dose parenteral steroid
and transitioned to oral steroid for lupus nephritis. She was also treated with primaquine and Malarone
(Atovaquone/proguanil) for possible Plasmodium vivax infection. At 1-week follow-up, her creatinine
remained stable and her appetite had improved.
[Date]
Discussion: Our patient had no symptomology of SLE and had a non-specific antibody work-up;
however, her renal biopsy was diagnostic for lupus nephritis. Great consideration was given to the
possibility of tropical nephrotic syndrome secondary to Plasmodium infection; however, renal biopsy
was not consistent with previously described histo-pathologic findings of malaria nephropathy. Our
case illustrates that SLE can present in the setting of systemic infections demonstrating the importance
of maintaining a broad differential diagnosis.
267
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Korosh Sharain, MD
But, The ANCA is Positive!
First Author: Korosh Sharain, MD Other Authors: Cyril Varghese, MD, Clement Michet, MD
CASE: A 62-year-old man with a history of type 2 diabetes presented to his local emergency department
with a worsening rash over his distal extremities. He described an unintentional 50-pound weight loss
and fatigue over the previous 6 months along with red-colored urine for the prior 3 weeks. He denied
any shortness of breath, nausea, abdominal pain, or fevers. Physical exam was notable for a known
aortic regurgitation murmur and a bilateral upper and lower distal extremity hemorrhagic bullous rash.
Labs were significant for an anemia to 10.3 g/dL, leukocytosis to 15.9x10(9)/L, and thrombocytopenia to
27x10(9)/L. His creatinine was elevated to 10.7 mg/dL from a baseline of 0.7 mg/dL and he was admitted
for hemodialysis. Further workup demonstrated schistocytes on blood smear, hypoalbuminemia,
positive c-antineutrophil cytoplasmic antibody (c-ANCA) and proteinase 3 (PR3) antibodies,
hypocomplementemia, and a positive rheumatoid factor. His presentation was concerning for vasculitis,
therefore, he was started on one gram of intravenous methylprednisolone. Unfortunately, his anemia
and thrombocytopenia worsened and his rash continued to spread proximally. He was then transferred
to our facility for plasma exchange. Upon transfer, his blood cultures from the outside hospital grew
gram positive cocci in chains and he was started on broad spectrum antibiotics. A subsequent
echocardiogram demonstrated supra-centimeter aortic and mitral valve vegetations. A Panorex was
negative. He also developed acute mental status changes and brain imaging was consistent with
multiple acute and subacute septic emboli. He required urgent aortic and mitral valve replacements
along with ceftriaxone for 6 weeks for Streptococcus mitis native valve endocarditis.
[Date]
DISCUSSION: This case highlights the importance of understanding the differential diagnosis of ANCA
positivity. Antineutrophil cytoplasmic antibodies are important markers for small vessel vasculitides;
however, prolonged infections including HIV, TB, and subacute bacterial endocarditis (SBE) can exhibit a
false positive ANCA and mimic vasculitis clinically, presenting a diagnostic and treatment challenge.
Small case series demonstrate that ANCA-positive SBE is often associated with hypocomplementemia
and a positive rheumatoid. Additionally, almost all cases of ANCA-positive SBE are c-ANCA and PR3
positive but p-ANCA and myeloperoxidase (MPO) negative. Also, ANCA-positive SBE has higher
morbidity and mortality compared to endocarditis without a positive ANCA, possibly due to delayed
identification and inappropriate initial treatment. Therefore, when vasculitis is considered, infection
must be ruled-out since immunosuppression could lead to dire consequences in an infected patient.
268
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Alan M Sugrue, MBBCh
Recurrent Spontaneous bilateral pneumothorax with thin walled cavities: A case
that leads to the scalp
First Author: Alan M Sugrue, MBBCh Other Authors: Chris Stephenson MD, Luke Hafdahl MD
Spontaneous bilateral pneumothorax is a rare and life threating condition. It is often associated with
underlying lung disease or malignancy, either primary or metastatic. A 75 year old male presented to
the emergency department complaining of shortness of breath, haemoptysis and chest discomfort for 3
weeks. He also described decreased weight loss of approximately 20 lbs over three months. He had a
past medical history significant for removal of an angiosarcoma from his scalp in April this year. He also
had bladder cancer s/p TURBT in 2013, prostate cancer s/p prostatectomy in 1995, Type 2 Diabetes,
COPD. He denied any infective symptomatology and review of systems was negative. He had a
significant smoking history of 83-pack year history.
His laboratory values on admission were within normal limits apart from a normocytic anaemia (Hb
10.5). On physical examining he was tachypneic with a respiratory rate of 30. Auscultation of the lung
showed decreased breath sounds of the right sided with hyperesonant percussion note. He had no
palpable lymphadenopathy; on his scalp he had a large incision from his recently removed
angiosarcoma.
Chest x-ray showed a right-sided pneumothorax with some cavitating lesions. While transferred to the
interventional radiology (IR) suite for a right chest drain, he become progressively more short of breath,
and was subsequently diagnosed with a new spontaneous left sided pneumothorax and had to have two
pigtail chest drains inserted on both the right and left side. While in the IR he also underwent a right
lung biopsy of one of the cavitating lesion.
His biopsy came with a diagnosis of metastatic angiosarcoma, with the primary lesion been from his
scalp. He was commenced on weekly taxane therapy. His hospital course was complicated by multiple
recurrences of a left sided pneumothorax, which we treated with a Heimlich valve (one way valve)
attached to his left sided chest drain, which enabled him to be discharged. Angiosarcoma are a rare
soft tissue sarcoma (2% of all sarcomas), they are highly malignant and are of vascular or lymphatic
epithelial origin. Angiosarcoma of the scalp has a predilection for pulmonary metastasis, classically
known to form thin walled cavities. The reason behind pneumothoracies remains obscure.. Prognosis is
poor with survival at 20% over two years with metastatic disease. Treatment is with taxanes based
therapy, with newer agents Pazopanib showing promise.
[Date]
The case highlights the rarely described association between metastatic angiosarcoma and spontaneous
pneumothorax, as well as the classically described thin wall cavities. It is extremely rare to develop
bilateral spontaneous pneumothoracies and it can be difficult to manage recurrent spontaneous
pneumothoracies in an ambulatory setting. Through the use of a Heimlich valve we are able to treat any
further recurrent pneumothoracies, while enabling him to return home, providing both benefits for the
patient and health care system.
269
MINNESOTA POSTER FINALIST - CLINICAL VIGNETTE Cyril Varghese, MD
Pneumonia Masquerading as a Rash
Cyril Varghese, MD, Korosh Sharain, MD, Matthew Koster, MD, and Clement Michet Jr., MD
Introduction: Mycoplasma pneumonia is a community-acquired infection that usually presents as an
upper respiratory tract infection. A constellation of cough, pharyngitis with atypical dermatological
and/or mucosal findings should prompt Mycoplasma antibody testing, even if a chest X-ray is negative.
In addition, having repeated pneumonias as a child or teenager should prompt testing for immunological
disorders.
Case: A 34-year-old man developed a sore throat and productive cough followed by a one-week history
of generalized rash, subjective fevers, injected eyes and intense myalgias. He did not report any sick
contacts or recent travels outside the United States. The patient reported to an urgent care center with
these symptoms two days later and was given a Medrol dose pack. His symptoms persisted, so he
presented to the hospital for further evaluation two weeks after developing symptoms. His past medical
history was significant for six episodes of pneumonia requiring hospitalization since childhood. Social
history was significant for regular marijuana use. On presentation, the patient was vitally normal and
stable with a diffuse morbilliform rash over his face, torso and extremities. He had conjunctival injection
and crackles at bilateral lung bases. He did not have any oral ulcers or tonsillar exudates. CBC was
significant for leucocytosis (WBC: 23.4X109/L with a left shift). However, infectious workup was negative
for Anaplasma, Ehrlichia, ASO, Lyme ELISA, RMSF AB, GAS PCR, HIV, Babesia, Adenovirus, CMV, EBV, and
measles virus and negative blood cultures. Rheumatological workup was negative for ANA, rheumatoid
factor, PR3, CCP AB, SSA/SSB, Sm AB, Scl 70, Jo 1 AB, Myeloperoxidase. Chest X-ray did not show focal
consolidation. However, his constellation of symptoms, including cough with sore throat, injected
cornea and atypical rash, prompted Mycoplasma pneumonia IgM and IgG antibody testing, both of
which were positive. His history of recurrent pneumonia in childhood and early adulthood warranted
further investigation with Complement levels, including C1q, C2, C3 and C4, all of which were low. The
patient was discharged on oral doxycycline and showed remarkable improvement of symptoms.
Discussion: Mycoplasma pneumonia usually presents as a self-limiting upper respiratory tract infection
[Date]
that has evolved into pneumonia, with the typical diffuse reticular interstitial findings on chest X-ray. In
rare cases, Mycoplasma pneumonia can present with other manifestations including morbilliform rash
or mucositis involving the eyes, genital, anal or oral mucosa. Although “walking pneumonia” is a
common presentation among young adults, having had repeated bouts of pneumonia during childhood
or young adulthood warrants further investigation. Dysregulation of complement activity can predispose
patients to autoimmune or infective process. Our patient had a mixed complement deficiency. In
general, deficiencies of the early components of the complement pathway (C1Q, C4 and C2) result in
autoimmune disorders like SLE. On the other hand, deficiencies in late complement components (C3-9)
lead to recurrent infections.
270
MISSISSIPPI POSTER FINALIST - CLINICAL VIGNETTE Lewis W Aldred, MD
Hypophosphatemia Masquerading as Meningitis
L W Aldred, MD M McCauley, MD J Pickett J O Knight M I Ullah, MD
Introduction: The differential diagnosis for altered mental status is vast, including drug overdose, meningitis,
intracranial lesions, and electrolyte abnormalities. Herein we report a case of severe hypophosphatemia
masked by a potential diagnosis of meningitis.
Case Description: A 68-year-old white female with rheumatoid arthritis and osteoporosis presented to the
emergency department after responders found her unresponsive on the floor of her bathroom. Initially, she
was obtunded and unable to provide any history. However, emergency physicians administered naloxone
with some response. After patient was awake, she complained of headache, photophobia, and “pirates
attack[ing] [her] ship.” Pertinent physical exam findings included tachycardia, photophobia, and a fentanyl
patch on her right chest. Investigative studies revealed a WBC count of 21.4 TH/cmm, as well as a urine drug
screen positive for benzodiazepines, opiates, and barbiturates. Other blood chemical levels drawn were as
follows: acetaminophen <15 mcg/mL, salicylate <1 mg/dL, and alcohol <10 mg/dL. Non-contrasted CT head
showed no acute intracranial abnormality. Initial differential diagnosis included polypharmacy as well sepsis
secondary to meningitis. We attempted lumbar puncture, but CSF was unable to be obtained. We initiated
ceftriaxone, vancomycin, and ampicillin as empiric coverage for meningitis. One day after admission, she had
a brief episode of witnessed seizure activity, which resolved with lorazepam. She remained confused 24
hours later with new onset bilateral vertical nystagmus. We ordered a complete electrolyte panel, which
revealed a serum phosphorus of 0.6 mg/dL and a drop in serum calcium to 7.7 mg/dL. A parathyroid
hormone level was found to be elevated at 278.3 pg/mL. IV phosphorous was given and the patient’s mental
status rapidly improved. Blood and urine cultures demonstrated no growth, and we discontinued her
antibiotics with no adverse events.
Further chart review showed that the patient had recently received an intravenous infusion of zoledronic acid
for osteoporosis 3 days prior to admission.
Discussion: This patient’s clinical presentation can be explained by her recent infusion of zoledronic acid.
Bisphosphonates cause mild to severe hypophosphatemia which can lead to metabolic encephalopathy. A
broad spectrum of neurological symptoms may be associated with severe phosphatemia ranging from mild
irritability and paresthesia to more severe manifestations such as delirium, generalized seizures, and coma. In
summary, in patients who meet SIRS criteria with altered mental status and no obvious source, meningitis
cannot be overlooked. However, it is prudent to keep electrolyte abnormalities in the differential diagnosis in
the face of high suspicion for meningitis.
References:


Alfred A. Reszka, Gideon A. Rodan. Mechanism of action of bisphosphonates. Curr Osteoporos Rep. 2003 September; 1(2): 45–52.
C. Berkelhammer, R. A. Bear. A clinical approach to common electrolyte problems: 3. Hypophosphatemia. Can Med Assoc J. 1984
January 1; 130(1): 17–23.
Silvis SE, DiBartolomeo AG, Aaker HM. Hypophosphatemia and neurological changes secondary to oral caloric intake: a variant of
hyperalimentation syndrome. Am J Gastroenterol. 1980;73(3):215-22.
Subramanian R, Khardori R. Severe hypophosphatemia. Pathophysiologic implications, clinical presentations, and treatment.
Medicine (Baltimore). 2000;79(1):1-8.
[Date]
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271
MISSISSIPPI POSTER FINALIST - CLINICAL VIGNETTE Doris K Hansen, MD
Physiologic Paraspinal masses in a patient with Hemoglobin C Disease
First Author: Doris K Hansen, MD; Clark Henegan MD, John Lam MD and Vince Herrin MD
Introduction: Extramedullary hematopoiesis (EMH) refers to the growth of hematopoietic tissue outside
of the bone marrow. EMH is a physiologic response to chronic anemia secondary to myeloproliferative
disorders or hemoglobinopathies. It is localized to the liver and spleen in 95% of cases; however, it may
also develop in paravertebral areas, especially the posterior mediastinum.
Here, we report a case where a patient was noted to have multiple paraspinal masses on imaging which,
upon biopsy, were found to be areas of EMH leading to a further diagnostic evaluation.
Case Report: A 73-year-old African American man was admitted for resection of an atypical lipomatous
tumor of the left thigh. On admission, he underwent Computerized Tomography (CT) of the Chest,
Abdomen and Pelvis to follow up a pre-operative Chest X-ray (CXR) concerning for hilar
lymphadenopathy. CT was notable for multiple paraspinal masses affecting the thoracic (T) spine at T8,
T9 and T10 as well as a spleen status post a prior partial resection. Biopsy of a paraspinal mass was
performed with pathology notable for extramedullary hematopoiesis concerning for a
myeloproliferative neoplasm versus a hemoglobinopathy.
Due to the patient’s underlying dementia, an extensive prior medical history was unable to be obtained.
He did, however, report a prior abdominal surgery after being “kicked by a mule.” Physical exam
demonstrated a midline abdominal vertical scar but no evidence of hepatosplenomegaly. He did not
have any palpable masses affecting the thoracic spine or any neurological deficits. Labs demonstrated a
normocytic anemia.
Patient declined a bone marrow biopsy. Hemoglobin electrophoresis was consistent with Hemoglobin C
Disease.
Discussion: In addition to the liver and spleen, paravertebral areas may be associated with EMH. Any
paravertebral mass consistent with EMH should prompt a clinician to consider an underlying
hemoglobinopathy in addition to myeloproliferative neoplasms. EMH is common in patients with
thalassemia and myeloproliferative disorders. However, only one literature case in Pubmed reports a
patient with Hemoglobin C disease and paravertebral EMH. Patients with Hemoglobin C Disease are
usually asymptomatic, have a mild degree of anemia with hemolysis and splenomegaly.
[Date]
Paraspinal extramedullary hematopoiesis may cause a variety of neurological symptoms depending on
size, location and if there is impingement of the spinal cord or nerve roots. More than 80% of patients
remain asymptomatic and the masses are typically discovered incidentally by radiologic imaging. Early
diagnosis is essential to rule out malignant processes of the posterior mediastinum.
272
MISSISSIPPI POSTER FINALIST - CLINICAL VIGNETTE Brandon W Lennep, MD
Extracorporeal Membrane Oxygenation for Electrical Storm as a Complication of
Acute Myocardial Infarction
First Author: Brandon W Lennep, MD University of Mississippi Medical Center, Dept of Internal Medicine Other
Authors: John T Saxon, MD, FACP University of Mississippi Medical Center, Dept of Internal Medicine, Division of
Cardiology
Introduction: Cardiogenic shock and refractory ventricular tachycardia are known complications of acute
myocardial infarction that are associated with a high mortality rate. Treatment of these sequelae is challenging,
and prompt intervention is paramount to promote good outcomes. When cardiogenic shock or ventricular
tachycardias are refractory despite appropriate revascularization, mechanical circulatory support is an appropriate
treatment.
Case Description: A 36-year-old African-American female presented with acute onset of chest pain, and initial
electrocardiogram (ECG) demonstrated an acute anterior ST-elevation myocardial infarction. She was referred for
emergent coronary angiography, which revealed complete occlusion of the proximal left anterior descending (LAD)
coronary artery and occlusion of two distal branches of the first obtuse marginal coronary artery. The patient
underwent emergent percutaneous coronary intervention with manual aspiration thrombectomy in the LAD and
deployment of a bare-metal stent in the proximal LAD. Due to persistent hypotension throughout the procedure, a
dopamine infusion was initiated and an intra-aortic balloon pump was placed for support. Over the next 24 hours
she reported no chest pain, but serial ECGs demonstrated an evolving anterior infarct pattern and transthoracic
echocardiography showed depressed left ventricular systolic function with anterior and apical hypokinesis. 24
hours after admission, she developed ventricular tachycardia which was refractory to multiple direct-current
synchronized cardioversions as well as to dual anti-arrhythmic therapy with amiodarone and lidocaine. She was
then upgraded to full mechanical circulatory support with veno-arterial extracorporeal membrane oxygenation
(ECMO). During 96 hours of ECMO support, she suffered no further hypotension or ventricular arrhythmia. She
was successfully weaned from ECMO and treated with standard medical management of acute coronary syndrome
prior to being discharged home on hospital day #10.
Discussion: Mortality remains over 40% amongst patients who develop cardiogenic shock as a complication of
acute myocardial infarction, despite recent improvement brought about by widespread implementation of early
revascularization techniques1. Cardiogenic shock due to electrical instability presents a particularly difficult clinical
scenario when ventricular arrhythmias are refractory to anti-arrhythmic therapy. Under such circumstances,
temporary full cardiopulmonary support with veno-arterial ECMO has been used in some cases as a bridge to
recovery of myocardial function2,3. These initial reports of success with ECMO support, taken in conjunction with
the failure of the intra-aortic balloon pump to confer a mortality benefit as shown in the IABP SHOCK II trial 4,
demonstrate the need for further, more powerful clinical studies to determine whether ECMO may reduce
mortality in cardiogenic shock complicating acute myocardial infarction. Demonstration of such a mortality benefit
would represent arguably the most momentous development since percutaneous coronary intervention.
References:
Werdan K et al. Eur Heart J. 2014; 35: 156-167 (2) Ariza-Solé A et al. Rev Esp Cardiol (Engl Ed). 2013 Jun; 66(6):501-3 (3)Brunner M et
al. Am J Emerg Med. 2013 Feb; 21(2):467.e1-6 (4) Thiele H et al. N Engl J Med 2012;367:1287-1296
[Date]
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273
MISSOURI POSTER FINALIST - CLINICAL VIGNETTE Cristina Ipatii, MD
FINDING "NEO"
Cristina Ipatii MD, Sadashiv Santosh MD, Alexandre Lacasse MD Department of Internal Medicine, St
Mary's Health Center, St Louis MO
Anti-N-methyl-D-aspartate (NMDA) receptor antibody encephalitis mostly affects children and young
females. It presents as an acute and rapidly progressive psychosis leading to encephalopathy
and possibly death. An occult neoplasm can be present, a teratoma in most cases.
A 20 year-old African American female presented with subacute psychosis unresponsive to antipsychotic
treatment. Three weeks preceding presentation, she had significant agitation with insomnia and new
onset grand mal seizure with transient lower extremity weakness. Then, rapid disintegration of
language, decreased responsiveness, mutism, dyskinesia with catatonic features were observed. On
examination, patient was confused, nonverbal, restless with catatonic posturing and non-tracking fixed
gaze. Hyperreflexia and myoclonus of the lower extremitieswere present. Brain magnetic resonance
imaging (MRI) was unrevealing. Cerebral spinal fluid (CSF) analysis showed
lymphocytic pleocytosis and monoclonal gammopathy. Infectious, vascular and toxic causes were not
found. Electroencephalogram showed generalized slowing with occasional seizure activity. Both serum
and CSF anti-NMDA receptor antibodies werepositive. Pulse dose corticosteroid and immunoglobulins
were initiated, followed by plasmapheresis. Rituximab was then initiated given lack of clinical
improvement. Ultrasound, computed tomograpgy (CT) and MRI of the pelvis, chest CT and spinal
MRI did not reveal an occult teratoma. Unilateral oophorectomy failed to detect one as well. Egg
harvesting followed by second oophorectomy have been considered. To date, complete
neurological recovery has been achieved.
[Date]
Acute and rapidly progressive psychosis followed by encephalopathy should raise suspicion for both
infectious and non-infectious encephalitis including anti-NMDA receptor encephalitis. High index of
suspicion in the correct clinical scenario should prompt treatment initiation prior to confirmatory
testing. Further interventions should be pursued to find an occult teratoma. If not found or
removed, then long term immunosuppression and periodic imaging are indicated.
274
NEBRASKA POSTER FINALIST - CLINICAL VIGNETTE Maryam F Gbadamosi-Akindele, MD
Hidden over the counter risk: Omeprazole induced acute interstitial nephritis!
Maryam Gbadamosi-Akindele M.D, Adegboyega Olayode M.D, Nathan Birch,M.D.
Case: We present the case of a 74 year old male who was admitted with acute kidney injury found on
routine basic metabolic panel (BMP). Serum creatinine was 5.8 mg/dl, increased from a baseline of 1.6
mg/dl. Past medical history was significant for hypogammaglobulinemia and gastroesophageal reflux
disease (GERD). Significant diagnostic studies included proteinuria, a fractional excretion of sodium of
5.35% and a renal ultrasound showing elevated resistive indices. The patient was hospitalized for one
day while he was hydrated with fluids. BMP 4 days after discharge again showed an increased
creatinine of 5.6mg/dl. He was readmitted with laboratory findings significant for hematuria,
eosinophiluria, pyuria and eosinophilia which were consistent with acute interstitial nephritis (AIN).
Further in depth history revealed that the patient recently started taking omeprazole which he
purchased over the counter for the treatment of GERD. Review of literature revealed that omeprazole is
an etiology of AIN, thus it was discontinued. Follow up BMP nine days after discontinuation showed a
decline in serum creatinine to 2.8 mg/dl. Subsequent creatinine at one month and six months were
2.6mg/dl and 1.8mg/dl respectively. A diagnosis of omeprazole induced AIN was made on the basis of
the decline in serum creatinine after omeprazole was discontinued.
Discussion: Omeprazole is a common over the counter medication used in the treatment of GERD. AIN is
an adverse effect of omeprazole that is rare and not well recognized. Clinical presentation varies with
only a few patients presenting with the classic triad of fever, rash and eosinophillia. Laboratory findings
include hemeaturia, proteinuria, eosinophiluria and pyuria. Diagnosis is usually made clinically but can
be confirmed with renal biopsy. The exact pathophysiology of omeprazole induced acute interstitial
nephritis is unknown. The literature suggests that patients with an underlying immunological
abnormality such as our patient may be at increased risk. The treatment is to discontinue omeprazole.
The use of glucocorticoids is controversial; nonetheless, it is commonly used in the treatment of
omeprazole induced AIN.
Conclusion: Physicians should be cognizant of omeprazole induced AIN since omeprazole is a common
over the counter medication. This case highlights the importance of a thorough review of over the
counter medications which patients may not voluntarily disclose on routine history.
References:
1. Simpson IJ, Marshall MR, Pilmore H et al. Proton pump inhibitors and acute interstitial nephritis: Report and analysis of 15 cases. Nephrology
2006;11:381–385.
2. Ruffenach SJ, Siskind MS, Lien YH. Acute interstitial nephritis due to omeprazole. Am J Med 1992;93:472–473.
[Date]
3. Myers RP, McLaughlin K, Hollomby DJ. Acute interstitial nephritis due to omeprazole. Am J Gastroenterol 2001;96:3428–34231.
275
NEBRASKA POSTER FINALIST - CLINICAL VIGNETTE Rajesh Kunadharaju, MBBS
A Rare Case Of Sarcoidosis Presenting As ARDS And Maculopapular Rash
First Author: Rajesh Kunadharaju, MBBS Second author: Sriharsha Tella.
Sarcoidosis is a multisystem inflammatory disease that is characterized by non-caseating granulomas on
pathology. It involves the skin in about 25% of cases, most common lesions being erythema nodosum,
maculopapular eruptions, subcutaneous nodules and lupus pernio. Lung involvement occurs in over 90%
of patients with sarcoidosis and classically manifests as bilateral hilar adenopathy although it can
present in a variety of ways. We describe a rare initial presentation of sarcoidosis as acute respiratory
distress syndrome (ARDS) and maculopapular eruptions.
CASE: A 55-year-old Caucasian male with a past medical history of sleep apnea, multiple back surgeries
and hypogonadism presented to the emergency room (ER) for 10 days of worsening shortness of breath
that coincided with new onset maculopapular rash that started from his penis. Rash was non-itchy,
painless and was initially noted in his penis that spread to his torso. He had no recent traveling overseas
except for being in Mexico for 3 weeks’ vacation 8 months ago, no animal contact, no recent changes at
home or relocating and he had not lived on a farmland. He has had the same partner for 8 months with
no new sexual contact. In the ER, patient was tachypneic and hypoxic with O2 saturation of 79% on
ambient air. PaO2/FiO2 ratio was 186mmHg and chest radiograph and CT showed bilateral interstitial
infiltrates with normal BNP and echo consistent with an ARDS picture. Bronchoalveolar lavage did not
show any evidence of infection including viral, bacterial, PCP, acid fast bacilli, fungi, or malignancy.
Alveolar hemorrhage was not noted. Skin biopsy came back as consistent with sarcoidosis. Patient was
treated with supportive measures and was started on prednisone with improvement of symptoms. He
was discharged home on 2 liters of oxygen. Upon outpatient follow up, rash had subsided and he had
much improved.
[Date]
DISCUSSION: The initial presentation and natural course of sarcoidosis can vary greatly. Lung
involvement is common but the development of ARDS as a manifestation of sarcoidosis has not been
well documented with only one case report in the literature. Our patient met the diagnostic criteria for
ARDS and the diagnostic tests performed did not reveal any other causes. This case outlines a rare but
potentially fatal presentation of sarcoidosis as ARDS. The importance of this report is primarily related
to the possibility that sarcoidosis may present as ARDS which, in the absence of an appropriate diagnosis
and treatment, could potentially be fatal. As far as we are aware, there has only been one case report of
acute life threatening pulmonary sarcoidosis presenting with ARDS.
276
NEVADA POSTER FINALIST - CLINICAL VIGNETTE Pannaga G Malalur, MD
Neurotoxicity of High Dose Intrathecal Gadolinium for CT Myelogram
First Author: Pannaga G Malalur, MD Second Author: Peter C. Rajacic, MD Third Author: Samir Patel, MD
Introduction There is a small but growing body of literature regarding the administration of low-dose
intrathecal gadolinium for various indications of contrast enhanced myelography and cisternography.
Although currently an off-label use, there is active discussion to gain FDA approval for such procedures.
A few case reports have noted adverse effects with accidental administration of high-dose intrathecal
gadolinium.
Case Description We report a 70 year-old male with past medical history significant for multiple spinal
surgeries who presented with altered mental status and bilateral hearing loss following a CT myelogram
using intentional administration of high-dose (12 cc) intrathecal gadolinium. Intrathecal gadolinium and
CT myelogram were utilized due to documented iodine allergy and presence of spinal hardware,
respectively. Lumbar puncture revealed elevated protein. MRI of lumbar spine without contrast showed
fluid collection in L4-5 region and diffuse hyper-density in the CSF. High dose IV dexamethasone, IV
fluids, IV antibiotics and acyclovir were started. Further workup ruled out infectious and aseptic
meningitis, infectious encephalopathy, encephalitis, and hypothyroidism. Repeat L-spine MRI displayed
resolution of the fluid collection and diffuse hyper-density. Also, repeat lumbar puncture noted a
downtrend of protein. The patient’s symptoms resolved prior to discharge. The most likely etiology was
an adverse reaction to high-dose intrathecal gadolinium.
[Date]
Discussion Limited experience in animal studies, case reports and human studies have demonstrated
the short and long term safety of administration of low dose (0.5 – 1 cc) intrathecal gadolinium in the
lumbar spine. However, the overall general safety has not been fully established and dosing guidelines
are ambiguous. The few case reports examining adverse reactions to higher doses suggest that
supportive therapy such as IV fluids, in combination with IV steroids and CSF drainage, is beneficial. The
fact that our patient improved with supportive treatment, IV steroids, and two lumbar punctures
reinforces the utility of this treatment. To our knowledge, this is the highest dose of intrathecal
gadolinium intentionally administered to a patient. Also as far as we can determine, this is the first
reported case where intrathecal gadolinium was used in a CT myelogram. It is unclear if serum/CSF
levels of gadolinium correlate with symptoms and if measuring the same would have clinical or
prognostic value. Our case in question may point to the eventual determination of protocols for patients
who cannot use iodinated contrast and cannot undergo MRI studies; and also to suggest treatment for
patients developing symptoms after gadolinium administration.
277
NEVADA POSTER FINALIST - CLINICAL VIGNETTE Susil Sivaraman, MD
An Unusual Cause for Left Ventricular Systolic Dysfunction: A Problem with Packing
First Author: Susil Sivaraman, MD Co-Authors: Swetal Patel MD, Eyas Chakfeh MD, Susanth Sivaraman
MD, Anthony Salem MD
Introduction: Heart Failure is a common medical condition affecting approximately 5.7 million
Americans. The most common causes for systolic heart failure in developed countries are ischemia,
hypertension, and valvular heart diseases. However, various other causes of heart failure are often
missed or overlooked. Our evaluation led to a diagnosis of a rare congenital cause for heart failure.
Case Description: A 59 year old Caucasian male with a past medical history of COPD, hypertension,
dyslipidemia, and frequent premature ventricular contractions presented with complaints of shortness
of breath and pedal edema. Physical examination showed an obese elderly male in acute respiratory
distress. He was afebrile with a pulse of 50 beats/minute, respiratory rate of 26/minute, BP of 180/105,
and saturation of 96 % on 2L nasal cannula. Other findings included an elevated JVP, bilateral basilar
crackles, and bilateral 2+ pedal edema. Electrocardiography showed bradycardia with trigemy and
frequent PVC’s. There were no ST changes. Echocardiogram demonstrated global left ventricular
hypokinesia, an ejection fraction of about 45-55%, and no valvular or septal defects. He underwent a
left heart catheterization, left ventriculography, and a coronary angiography. The ventriculography
confirmed an LV ejection fraction of 40%. Coronary angiography showed non-flow limiting, nonobstructive coronaries. All investigations failed to identify the cause of his left ventricular dysfunction.
The patient was labeled with “non-ischemic cardiomyopathy” and managed with standard heart failure
medications.
He was admitted to our hospital six months later with worsening dyspnea on exertion. Contrast
echocardiogram showed a worsening ejection fraction of 30%. The contrast was found penetrating the
left ventricular myocardium revealing recesses in the left ventricular apex. This is pathognomic of a rare
congenital cardiac condition known as “non-compaction cardiomyopathy”.
He was placed on maximum medical therapy, and planned for ICD placement due to the increased risk
of ventricular arrhythmia and sudden cardiac death. His first degree relatives were also screened for
NCCM.
[Date]
Discussion: This case emphasizes the importance of re-evaluating a patient, and keeping an open mind
to even the rarest of conditions. Non-compaction cardiomyopathy (NCCM) is a rare congenital condition
(prevalence estimated at 0.05%-0.24%), that occurs from an arrest of normal myocardial compaction
during embryonic development. This results in increased trabeculations and intertrabecular recesses
within the myocardium. Diagnosis is primarily based on morphological findings of NCCM. There is no
specific management for NCCM; patients should be treated for heart failure, arrhythmias, and
thromboembolic events per standard guidelines. NCCM has also been tied to many different gene
mutations. Therefore, the Heart Failure Society of America recommends echocardiographic screening of
all first degree relatives.
278
NEW HAMPSHIRE POSTER FINALIST - CLINICAL VIGNETTE Khushboo Shah, MD
Jehovah's Witness with a Triple-Hit: Beta-Thalassemia Trait + Paroxysmal
Nocturnal Hemoglobinuria (PNH) + Chronic Myeloid Leukemia (CML)
Khushboo A. Shah, MD (1); Peter Kebbekus, MD, PhD (2); Spencer L. James, MPH (3); Joseph Shatzel, MD (1);
Evelyn Brosnan, MD, MBA (1), Khushboo A. Shah, MD (1); Peter Kebbekus, MD, PhD (2); Spencer L. James, MPH (3);
Joseph Shatzel, MD (1); Evelyn Brosnan, MD, MBA (1) , 1. Dartmouth-Hitchcock Medical Center, Lebanon NH, 2.
Norris-Cotton Cancer Center, Lebanon NH, 3. Geisel School of Medicine at Dartmouth, Hanover NH
Introduction: Paroxysmal Nocturnal Hemoglobinuria (PNH) is a benign hematopoetic clonal stem cell
disorder characterized by a somatic mutation of the PIGA gene that renders these cells prone to
hemolysis. This mutation alone however, is insufficient to account for the clonal dominance necessary for
clinically apparent PNH. While immune mechanisms have been thought to mediate clonal selection of PNH
cells several reports have postulated the idea of a second, driver mutation that would provide a strong
survival advantage for PNH to become clinically apparent. Here we report a case of a Jehovah's Witness with
Beta-Thalassemia Trait who was diagnosed with Paroxysmal Nocturnal Hemoglobinuria (PNH) and a year
later was discovered to have Chronic Myeloid Leukemia (CML). His religious aversion to blood products
added additional complexity to his already challenging case.
Case Presentation: A 52-year old male Jehovah’s witness with a past medical history of Beta-Thalassemia
trait presented with a several week history of significant fatigue and jaundice. His CBC was notable for a
profound microcytic anemia (Hb 5.9) with a normal differential. Hemolysis labs were positive with a negative
Coomb's test. Blood flow cytometry revealed deficiency of glycosylphosphotidylinositol anchor (GPI-A)
bound proteins on ~50% of erythrocyte & lymphocyte populations consistent with PNH. Treatment with
Eculizumab, a humanized monoclonal antibody targeting C5 terminal complement activation, was initiated.
The initial response to treatment was dramatic with significant improvement of his hemolysis
markers. About 1 year into treatment, the patient complained of returning fatigue. Labs were remarkable
for a persistently elevated reticulocyte count of >20%, progressive thrombocytosis of >1,000,000 with a rising
leukocytosis. Bone marrow biopsy revealed the presence of Philadelphia (Ph) chromosome and BCR-ABL
translocation by RT-PCR and FISH, confirming the diagnosis of a superimposed chronic myeloid leukemia
(CML). Treatment with Imatinib, a tyrosine-kinase inhibitor, was initiated and after just 6-8 months, both the
BCR-ABL/ABL ratio and PNH clone population were no longer detectable. Eculizumab therapy was stopped
and the PNH clone remained undetectable on all subsequent testing. Remarkably, all of his cell lines are
within normal range and he averted requiring any blood product transfusions since his initial diagnosis.
Discussion: Does the patient have two separate clones, one harboring the PIGA mutation and another
harboring the BCR-ABL translocation, or was there just one clone with both mutations present? This
question was particularly important for a Jehovah’s witness who would not accept transfusion support and
may be dependent on a CML clone for normal erythropoiesis in the 2-clone scenario.
[Date]
While there is no direct evidence to support either theory, we suspect there was just one clonal stem cell
harboring both the PIGA mutation and BCR-ABL translocation. The hypothesis supported by
coinciding improvement in the patient's CML disease with Imatinib with the disappearance of the patient's
PNH clones. In fact, the patient was able to stop taking Eculizumab with no recurrence of PNH almost 4 years
279
later. It's unclear if the original PNH clone found at first presentation harbored a yet indolent BCR-ABL
mutation or if a BCR-ABL mutated clone provoked the PIG-A mutation responsible for development of PNH.
[Date]
The case highlights a uniquely challenging situation for a Jehovah’s witness faced with three simultaneous
blood disorders: CML, PNH & underlying Beta-Thalassemia Trait. This is an extremely uncommon event that
to our knowledge has never been reported before. Further studies are required to clarify the pathogenetic
relationship between CML and PNH.
280
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Martin Miguel I Amor, MD
AORTICO-LEFT ATRIAL FISTULA: A RARE COMPLICATION OF INFECTIVE
ENDOCARDITIS
First Author: Martin Miguel I Amor, MD Abhinav Agrawal MD, Deepa Iyer MD, Marc Cohen MD
INTRODUCTION: Paravalvular aortic root abscess with intracardiac fistula formation is an exceedingly
rare complication of infective endocarditis. This complication places patients at increased risk for
congestive heart failure, heart block and death.
CASE DESCRIPTION: A 68-year-old Bosnian female with prior aortic valve replacement with a
bioprosthetic valve for aortic regurgitation was admitted for worsening shortness of breath, fever and
lethargy. She was recently on a vacation in Bosnia, where she fell ill and was hospitalized for 1 month for
sepsis and renal failure. She had an extensive past medical history, pertinent for coronary artery disease,
s/p PCI and stenting, diastolic congestive heart failure, atrial fibrillation, chronic kidney disease, systemic
hypertension, multiple prior cerebrovascular accidents and chronic UTI. In the ED, she became markedly
hypotensive and hypoxic. She was intubated and started on dopamine infusion. A bedside transthoracic
echocardiogram revealed a paravalvular leak around the bioprosthetic valve, raising concern for an
aortic root abscess. EKG revealed atrial fibrillation with low voltage QRS, without evidence of bundle
branch blocks or conduction delays. The patient developed septic shock and was started on broad
spectrum antibiotic therapy and pressor support. A transesophageal echocardiogram revealed an
extensive aortic root abscess. The abscess had ruptured into the left atrium, with a fistula connecting
the aortic root to the left atrial cavity. The abscess was located around the bioprosthetic aortic valve
which had a large vegetation and severe paravalvular aortic regurgitation. She became
hemodynamically unstable during the procedure and was brought to the operating room for emergent
surgery. She underwent homograft aortic root replacement, VSD repair and ligation of the aortico-left
atrial fistula. Two sets of blood cultures grew Enterococcus faecalis. Postoperatively, she developed
worsening septic shock, requiring multiple pressors, disseminated intravascular coagulation, and anuria,
requiring CVVHD. She eventually expired 5 days later.
[Date]
DISCUSSION: Intracardiac fistula formation is a rare and particularly problematic complication of
periannular spread of infective endocarditis, with high mortality despite adequate therapy. In prosthetic
valves, this process usually begins on the prosthesis cuff, and often extends outside the valvular
apparatus, resulting in valvular dehiscence, abscess formation, and myocardial involvement. Operative
treatment remains the cornerstone of management. Surgical treatment involves removal of all infected
tissue including annular elements, followed by reconstruction of the annulus for safe anchoring of a
valve conduit. Early rather than delayed surgical intervention has been shown to improve survival. In our
patient, a delay in the diagnosis, which in turn led to a delay in surgical intervention, contributed to the
poor outcome. This case illustrates that a high index of suspicion, prompt diagnosis by
echocardiography, and early rather than delayed surgical intervention, are crucial to improving
treatment outcomes for this rare condition.
281
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Anteneh Birru, MD
Idiopathic thromboembolism and occult malignancy
First Author: Anteneh Birru Second Authors: Daniel Goldsmith, MD. Emily Chen, MD
Introduction The association between venous thromboembolism (VTE) and occult malignancy was well
established more than a century ago. Studies report a 10% malignancy incidence in patients with
idiopathic VTE who were followed over two years. However, there are no clear clinical guidelines on
evaluation of patients with idiopathic VTE for occult malignancy.
Case Presentation A 56 year old African American male with a history of hypertension, diabetes mellitus,
and hyperlipidemia, presented with complaints of left leg pain and swelling for three days. He denied
any trauma, shortness of breath, chest pain, palpitations, fever, chills, abdominal pain, recent travel and
prior similar events. He reported involuntary weight loss of 10 lb over the last three months. Vital signs
were temperature 98.8 F, pulse 90 bpm, respiration 16/min, oxygen saturation 99%, and blood pressure
117/77 mmHg. The left lower extremity showed diffuse swelling below the knee and was tender to
palpation. Laboratory evaluation showed hemoglobin of 6.9 mg/dL, hematocit 22.3%, WBC 11 and
platelets 294. Doppler image of the lower extremities revealed extensive acute deep vein thrombosis in
the left proximal to distal femoral, popliteal, and tibial veins. Subsequently, the patient underwent
inferior vena cava filter placement due to the low hemoglobin. Iron studies for anemia showed iron
deficiency. The patient was transfused 2 units of PRBC’s. On day 2 of admission, CT of chest, abdomen,
and pelvis images revealed pulmonary embolism and a 7.8 x 7.9 x 8.6 cm right colon mass. On day 4,
colonoscopy showed a polyp and a 3mm apple core lesion in the right colon. Later, the patient
underwent right hemi-colectomy and pathology reported invasive, moderately differentiated
adenocarcinoma of the colon without metastasis. Further adjuvant chemotherapy wasn’t initiated due
to tumor stage (T2NO). The patient was started on heparin and bridged to warfarin. Given an early and
thorough investigation for an idiopathic thromboembolic event, an occult malignancy was revealed and
treated early.
Discussion A first episode of idiopathic VTE may herald an occult malignancy. There is still some
uncertainty whether screening for malignancy improves prognosis in such a patient group. However,
early detection of occult malignancy has a positive association with increased treatment possibilities and
survival. VTE patients should be investigated for age and risk factor appropriate malignancies, and all red
flag abnormalities must be fully evaluated. In our case, even if the CT scan had not revealed a mass, the
patient would have been appropriate for an early colonoscopy because of the anemia.
[Date]
Learning point Until there are clear clinical guidelines available for evaluation of occult malignancy in
idiopathic VTE patients, it is important for clinicians to diligently look for occult malignancy with
thorough medical history, physical examination, directed laboratory tests and imaging.
282
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Ria D'Souza, MD
Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis associated with ovarian
teratoma: a challenging diagnosis
First Author: Ria D'Souza Second Authors: Julius Salamera, Stephen Sachs, Sonia FNU, Naresh Joshi
Anti-NMDAR encephalitis is a paraneoplastic encephalitis associated with anti-NMDAR antibodies, first
reported in 1997. It is most commonly seen in young women with ovarian teratoma, as well as in men
and children. Some of the characteristic clinical features include bizarre dyskinesia, epileptic seizures,
hypoventilation, neuropsychiatric manifestations, and decreased level of consciousness.
A 25-year old French woman with no medical or psychiatric history was brought in from Newark Liberty
International Airport due to acute mental status changes. She was travelling with her boyfriend and
younger sister from Belgium to United States for a leisure trip. The patient was noted to be acutely
agitated on the plane, evidenced by incoherence of speech, and attempting to open the cockpit door.
On arrival, she exhibited bizarre behavior with uncoordinated movements. As per patient’s boyfriend,
there was no history of alcohol or substance abuse. Urine drug screen, alcohol, and ammonia level were
negative. Psychotropic medications did not improve her mental well-being. A CT scan as well as MRI of
brain did not show any acute pathology. A diagnostic lumbar puncture has CSF lymphocytic pleiocytosis,
with normal opening pressure, glucose, and protein. EEG revealed mild, diffuse slowing. Empiric
acyclovir was initiated pending CSF work-up. Blood, urine, and CSF cultures were negative. Fungal, viral,
and acid fast bacilli culture were also negative. Cytology has no malignant cells. Patient clinically
deteriorated with acute urinary retention, and acute hypoxic respiratory failure from aspiration
pneumonia. A CT scan of the chest, abdomen, and pelvis disclosed multilobar consolidation, and
distended urinary bladder up to umbilicus. CSF studies including PCR for HSV 1/2, West Nile virus, Lyme,
VDRL, 14-3-3 protein, myelin basic protein, oligoclonal bands, and cryptococcal antigen were negative.
HIV antibody, interferon gamma release assay, and ANA were also negative. She was started on high
dose steroids due to concern for autoimmune encephalitis, which was then tapered with modest
improvement. A repeat CT of the abdomen and pelvis revealed a left ovarian mass suggestive of ovarian
teratoma with positive serum anti-NMDAR antibodies on CSF. She underwent resection of ovarian
teratoma, with concurrent intravenous immunoglobulin therapy. Currently, the patient has improved
neurologically following a trial of rituximab and cyclophosphamide.
[Date]
Anti-NMDAR encephalitis and its association with ovarian teratoma in young women is still a relatively
unknown diagnosis. The diversity of symptoms frequently results in misdiagnosis as a psychiatric,
infectious or toxicological process. Emergency physicians and Internists must consider the diagnosis
when a young female patient presents with acute mental status changes, dyskinesia, and new onset
seizures, in whom toxicological and infectious etiology has been ruled out. Treatment includes resection
of ovarian tumor and immunotherapy. Avoiding diagnostic delay will result in early initiation of
immunotherapy and tumor resection, which has been associated with improved outcomes.
283
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Mufaddal Q Dahodwala, MD
Indolent DRESS Syndrome: The Calm Before The Storm
First Author: Mufaddal Q Dahodwala, MD Second Author: David J Ross, MD
We present a case of Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) that highlights
the potential harm of seemingly benign environmental insults in a patient whose immune milieu is
heightened.
A 29 year-old South Asian woman with asthma, eczema, and back pain presented to the ICU after three
weeks of progressive fever, profuse watery diarrhea, and rash. She ingested oysters two days prior to
symptom onset, and while others in her party suffered 24-hour GI upset, her symptoms progressed.
Home medications included oral contraceptives, albuterol, NSAIDs, and herbal supplements. Her exam
was notable for fever, anasarca, normal buccal mucosa, no significant adenopathy, tachycardia, and
generalized moribilliform papular rash over trunk and all extremities, with sparing of palms and soles.
Admission labs were notable for leukocytosis, monocytosis, and depleted electrolytes. Skin biopsy
showed perivascular lymphocyte-predominant inflammation with dermal edema. During her admission,
her fevers and abdominal pain progressed. A broad diagnostic workup was largely negative, except for
positive serum Strongyloides antibodies, positive antitransglutaminase, and positive HTLV screen and
antibody. Her liver function deteriorated, with peak AST 2136, ALT 1304, and MELD 26. Serum IgE
peaked at 20,827, and she developed peripheral eosinophilia. Liver biopsy suggested acute hepatitis or
drug-reaction. Serum EBV, hepatitis panel, and HHV-6 PCR were negative. She was diagnosed with
DRESS, presumably secondary to chronic NSAID or herbal supplement use followed by a subsequent
trigger exposure to oysters or antibiotics. She was treated with IVIG and IV steroids, after which she
defervesced, her rash nearly resolved, her liver tests normalized, and her anasarca improved. Notably,
she later received ketorolac for abdominal pain during the admission. The next morning, her rash
returned, now involving oral mucosa, and progressed to 100% BSA. Repeat skin biopsy was suggestive of
SJS/TEN. She was transferred to a burn center, where she developed Pseudomonal sepsis, and passed
away four days later.
[Date]
This tragic case highlights the nefarious potential of a DRESS reaction, even when initially indolent.
Culprit exposures are difficult to identify, and in this case while NSAIDs and herbal supplements are
more likely given that symptoms usually begin 2-6 weeks after an exposure, we will likely never know.
Current recommendations support early systemic steroids, though no randomized clinical trial data exist
investigating long-term outcomes with this strategy. In this case, given the positive Strongyloides tests,
it was critical to rule out infection before starting steroids, as symptoms can often look similar. Finally,
this is a unique case given that the patient suffered from both DRESS and SJS/TEN in a short time period,
two separate clinical entities that may not have been related to a single exposure, given the fast time
course and distinct histopathologic characteristics.
284
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Joseph DeRose, DO
Human Granulocytic Anaplasmosis in the Setting of a Hunting Injury
First Author: Joseph DeRose, DO
Human Granulocytic Anaplasmosis is a traditionally tick borne illness characterized by non-specific
symptoms. Most cases occur in spring/summer in the Northeastern and northern Midwest US.
63 year old man with medical history of HIV on ART, presented to EO-VAMC with a complaint of cyclic
fevers, chills, and diarrhea. Symptoms began with generalized weakness one week prior to presentation.
Patient revealed he was a hunter and experienced trauma to his hand while butchering a deer. Diarrhea
began four days prior to presentation with multiple bowel movements associated with lack of appetite,
abdominal discomfort and nausea. He denied vomiting, hematemesis, sick contacts, changes in diet,
shortness of breath, recent travel or known tick exposure. On physical exam patient was tachycardic, illappearing and over short period of time became hemodynamically unstable and was admitted to MICU.
Initial labs were significant for thrombocytopenia, coagulopathy and transaminitis. He was fluid
resuscitated and Infectious Disease service was consulted. He was started on broad spectrum antibiotics
given his recent hunting injury and possible tick exposure. The patient’s clinical status improved
throughout his hospital stay and he was discharged on Azithromycin, Atovoquone and Doxycycline. The
patient returned to ID clinic two weeks after discharge and reported complete resolution of symptoms.
Titers at that time revealed (+) IgM against HGA and re-examination of the peripheral smear revealed
intraleukocytic morulae characteristic of Erlichia/Anaplasmosis infection. Given patient’s history of
trauma while butchering a deer, timeline of symptoms and positive Anaplasmosis serology, diagnosis of
HGA with transmission via handling of infected butchered deer meat was made.
[Date]
This case illustrates an uncommon mode of HGA transmission and emphasizes value of obtaining
thorough history. Although the mode of transmission in this case is rare, the disease is common to the
northeast US and recognition, prompt treatment is necessary to prevent complications.
285
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Prerna Dogra, MBBS
DRAMATIC RESPONSE TO INFLIXIMAB IN REFRACTORY NEUROSARCOIDOSIS
COMPLICATED BY CRYPTOCOCCAL MENINGITIS
First Author: PRERNA DOGRA PARAG CHEVLI, ROBIN PAUDEL, SAURAV SUMAN, VALENTIN MARIAN
INTRODUCTION: Neurologic involvement occurs in approximately 5% of patients with sarcoidosis.
Corticosteroids are considered first line agents for treatment but patients who deteriorate despite
aggressive corticosteroid treatment, cannot tolerate corticosteroids, or have a primary contraindication
to corticosteroids may benefit from alternative immunosuppressive therapies. We report a case of
refractory neurosarcoidosis complicated with cryptococcal meningitis that showed dramatic
improvement in clinical and radiological manifestation after treatment with Infliximab. CASE
DESCRIPTION: A 44 year old African American female presented with two weeks of progressive left sided
hearing loss and facial droop associated with gait imbalance. MRI of brain showed ring enhancing lesions
and CT scan of the chest was significant for bilateral hilar lymphadenopathy. After extensive work up
including biopsy of right lung showing non-caseating granulomas and excluding other granulomatous
inflammatory, infectious and malignant etiologies, patient was given a diagnosis of pulmonary and
neurosarcoidosis. She was started on treatment with prednisone and discharged. After two weeks, she
presented with lethargy and fever of 102 F. MRI of brain showed improving brain lesions but lumbar
puncture was significant for positive Indian Ink stain and elevated Cryptococcal Antigen (CAg) titers. She
was started on stress dose hydrocortisone along with two weeks of induction therapy with
Amphotericin and Flucytosine. Due to failure to improve after 10 days, induction therapy was continued
for another four weeks along with serial lumbar puncture every 48 hours. After four weeks of induction
therapy, there was no improvement along with persistently high CAg titers and opening pressures. MRI
of Brain was performed which showed unfavorable progression of brain lesions and it was believed that
patient had worsening of neurosarcoidosis along with cryptococcal meningitis leading to failure in
improvement. It was decided to start treatment with Infliximab infusion. After first dose of Infliximab,
slight improvement in mental status was noted with decreasing CAg. Following second and third
infliximab infusion patient showed dramatic improvement in mental status along with resolving
meningitis. A repeat MRI of brain revealed significant improvement along with resolution of lesions in
multiple areas. The induction therapy was completed and maintenance therapy with fluconazole was
started. Patient was then discharged with outpatient infliximab infusions.
[Date]
DISCUSSION: This case represents the difficulty in managing neurosarcoidosis especially in patients
where the course is complicated with life threatening opportunistic infection. Intriguing is the fact that
our patient improved dramatically with Anti-TNF-alpha therapy, including cryptococccal meningitis
which was refractory to anti-fungal therapy alone thus reinforcing the existence of an immune relation
between sarcoidosis and cryptococcosis. Clinicians should be vigilant about this association and the fact
that treatment of sarcoidosis may improve immune-response against cryptoccocus.
286
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Rishi Handa MD
Charcoal Heart - Cardiac Metastasis of Malignant Melanoma
First Author: Rishi Handa MD Second Author: Ashwini Arjuna MD Third Author: Carly Fabrizio MD Forth
Author: Arshi Handa MD Fifth Author: Joel Maslow MD
Malignant melanoma (MM) is a neoplasm with one of the most unpredictable biological behaviors,
including cardiac involvement. Most cases of cardiac metastasis are clinically silent and are rarely
identified ante-mortem. However, when they do manifest patients often present with life threatening
non-specific cardiac morbidities including heart failure, pericardial effusions, outflow tract obstructions,
or arrhythmias. Here we present a case of cardiac metastasis of MM.
The patient is a 64-year-old Caucasian female with history of MM of the right lateral chest wall that was
status-post wide excision with adjunctive post-operative immunotherapy in 1994. The patient now
presented to the hospital 8 years later with complaints of increasing dyspnea on exertion and chest
discomfort for 5 days. During the patients initial hospitalization she underwent computed tomography
(CT) of the chest to rule out pulmonary embolism and was incidentally found to have a large pericardial
effusion consistent with tamponade, confirmed by echocardiogram. The patient received pericardial
window drainage via video-assisted thoracic surgery and was started on Celebrex. Drained fluid analysis
was performed and was negative for malignancy. The patient was discharged home with close follow-up
however, she again presented to the hospital with worsening shortness of breath and chest discomfort.
This time she had an elevated d-dimer and underwent repeat imaging which revealed bilateral pleural
effusions and a small pericardial effusion. Her pericardium appeared thickened and she was diagnosed
with constrictive pericarditis and was consequently started Colchicine and Celecoxib. The patient was
discharged and was arranged for close follow-up however, she subsequently presented with similar
symptoms. This time, she was found to have unprovoked bilateral pulmonary emboli and underwent IVF
filter placement, due to a history of bleeding GI ulcers. After having a negative hypercoagulable work-up
the possibility of malignant recurrence was pondered. Repeat ECHO and cardiac MRI now displayed a
mysterious intramural cardiac mass which was later found to be a metastatic melanoma lesion, verified
by thoracotomy biopsy and pathology and positive fluid cytology for malignancy on repeat testing.
[Date]
MM has a very high tendency to metastasize to the heart and it is important for clinicians to be alert to
the possibility of possible cardiac metastasis in patients even without clinical symptoms. As seen in this
case, drained fluid cytology may be negative for malignancy and early tissue biopsy may be
indicated. Furthermore, future utility of interval screening using echocardiograms to prevent advance
presentation of patients should be addressed.
287
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Inga Harbuz-Miller, MD
An obscure presentation of congenital heart defect in a septuagenarian lady.
First Author: Inga Harbuz-Miller, MD Melissa Mauro, MD Mubashir Ahmed, MD Jacqueline Darcey, MD.
Heart failure (HF) is very frequent in aging population and is sometimes more complex with aberrant
anatomy. Atrial septal defect (ASD) is a congenital heart defect which can avoid detection until
adulthood when secondary pathophysiologic changes develop. ASD repair in advanced age is often
associated with complications.
A 72-year-old woman presented with lethargy, hypoxemia and hypercarbia. Four years prior she had
ASD repair, tricuspid annuloplasty and left atrial appendage ligation. During the past year she had
multiple hospitalizations for respiratory failure; extensive evaluation ruled out URI, COPD, and
obstructive sleep apnea and a diagnosis of HF was made. Transthoracic echocardiogram ( TTE) showed a
reduced ejection fraction of 30% with combined systolic and diastolic dysfunction. She started
treatment with diuretics and required vasopressors and inotropic support. Noninvasiveventilation with
bipap was used for ventilator support but she remained hypoxemic even with radiographic and clinical
improvement. Repeat TTE with bubble study was granted to reassess ASD. Administration of contrast in
left cephalic vein was visualized traversing left atrium and left ventricle without ASD or VSD. Dedicated
computer tomography angiogram showed persistent left superior vena cava draining into an unroofed
coronary sinus and left atrium: a double right to left shunt from left superior vena cava and coronary
sinus. The patient was not a surgical candidate; medical management was optimized and with high-flow
oxygen her oxygen saturation was 88-90%.
[Date]
This illustrates that sometimes with advanced age clinical presentation with HF can conceal underlying
anatomical congenital defects that are less likely subject to discovery in septuagenarian population.
288
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Uzma Imran, MD
Recurrent abdominal pain, a difficult diagnosis of Behcet’s disease
First Author: Uzma Imran, MD. Beede MS,MD. Goldsmith D, MD.
Backgorund: Behcet’s disease (BD) is a multisystem inflammatory vasculitis, characterized by recurrent
oral and genital ulcerations, uveitis and frequently positive pathergy test. There can be a variety of
visceral manifestations, including articular, gastrointestinal and nervous system involvement, though
not frequently seen in the US population.
Case: A 34 year old Hispanic woman with a history of thrombocytopenia, was hospitalized multiple
times in the last 2 years due to recurrent abdominal pain, diagnosed as terminal ileitis and colitis.
Further investigation revealed a history of recurrent oral ulcers with a recent labial ulcer which
suggested a clinical diagnosis of Behcet’s disease, although she did not have uveitis symptoms and a
pathergy test was negative. Colonoscopy revealed a single punched out ulcer of the descending colon,
nonspecific acute inflammation with intact crypt architecture on histopathology, anti-Saccharomyces
cerevisiae IgA antibodies was minimally elevated 26.1(N <20). Labial ulcer biopsy revealed chronic
vulvitis with no dysplasia which supports our diagnosis. Interestingly she had chronic mild
thrombocytopenia with platelets <130,000 , which can be associated with Behcet’s. Colchicine and
azathioprine were attempted but discontinued due to intolerance. Intestinal flares have been reduced
and responded well to systemic steroids.
Discussion: The prevalence of BD is higher in Middle and East Asia than in Western countries. Intestinal
BD is a specific subtype of BD, characterized by intestinal ulcers and associated gastrointestinal
symptoms. Similar to inflammatory bowel disease, intestinal BD exhibits a fluctuating disease course
with repeated episodes of relapse and remission that necessitate adequate maintenance therapy after
achievement of clinical remission. Medical treatment of intestinal BD is largely empirical since wellcontrolled studies have been difficult to perform due to the heterogeneity and rarity of the disease. 5aminosalicylic acid, systemic corticosteroids, and immunosuppressants have been used anecdotally to
treat intestinal BD. The clinical course of intestinal BD shows considerable variability, and the exact point
at which more potent agents such as immunosuppressants should be used has not been elucidated.
Teaching point
[Date]
Refractory colitis should raise the suspicion of Behcet’s disease if Crohn’s disease is ruled out.
289
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Waqas Jehangir, MBBS
Multi-vessel Spontaneous Coronary Artery Dissection: A Diagnostic Challenge in an
Unlikely Setting
First Author: Waqas Jehangir, MBBS,MD Co-Author: Tarek Aly, Shuvendu Sen, Abdalla Yousif
Introduction: As a healthcare professional, anchoring heuristic is a diagnostic error that one must be
aware of when approaching every patient. This diagnostic error is the healthcare professional's
tendency to rely on a previous diagnosis, and in situations where a set of symptoms might mask a rare
and deadly condition, this error can prove fatal for the patient. One such condition, Spontaneous
Coronary Artery Dissection, is an uncommon and malefic presentation of coronary artery disease that
can lead to myocardial infarction and sudden death. Spontaneous Coronary Artery Dissection SCAD is
seen predominantly in women with a mean age above 40. In a young, athletic male with a SCAD, the
danger of diagnostic error is overwhelming due to the broad symptomatology and the betraying
demographic.
Case Description: A 27 year old man without any significant past medical history presented with a two
week history of intermittent, retrosternal, stabbing chest pain that radiated to his left arm and shoulder.
The pain was associated with nausea and diaphoresis. As the pain was pleuritic and positional, and the
patient had an upper respiratory tract infection with fever and chills prior to the onset of the pain, his
primary care physician had made the clinical diagnosis of costochondritis. The patient was a physically
active, young male who denied alcohol use, smoking, or illicit drug use. While engaged in a sporting
activity, the pain became exacerbated and the patient was admitted due to concern for a cardiac cause
of the distress. On physical examination, patient was tachycardic and tachypneic while his blood
pressure and other findings were unremarkable. His initial lab results showed leucocytosis. Follow up
ECG showed ST elevation in anterolateral leads which prompted a cardiology consultation. After
consultation, the emergency physician called a Code Heart and the patient was sent to the cardiac
catheterization lab for rescue angioplasty. He was found to have a 95% mid Right Coronary Artery RCA
dissection with a total Left Anterior Descending LAD artery spontaneous dissection while all other
remaining vessels were found to be normal. Percutaneous Coronary Intervention to the LAD and mid
RCA was performed with intra-aortic balloon pump placement.
[Date]
Discussion: The initial diagnosis of costochondritis made by the primary care provider was the diagnostic
formulation that could have influenced future judgments made in the therapeutic plan. This example
presents the danger of anchoring heuristic as this patient did not fit the clinical demographic of SCAD
and the diagnosis of costochondritis could have delayed pivotal interventions that could have been life
saving. Chest pain must always be taken into serious consideration and Acute Coronary Syndrome
should always be ruled out regardless of the presenting demographic.
290
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Mohleen Kang, MD
Spontaneous Hemoperitoneum as an Initial Manifestation of Plasma Cell Leukemia
First Author: Mohleen Kang Other Authors: Nitasha Bhatia and Mirela Feurdean
Introduction: Plasma Cell Leukemia (PCL) is a rare but aggressive variant of multiple myeloma which
either presents as a progression of multiple myeloma or as primary PCL. It typically presents with
anemia, leukocytosis, acute renal failure, hypercalcemia, lytic bone lesions and in some cases with
hepatosplenomegaly. We present a case of plasma cell leukemia presenting with spontaneous splenic
bleeding.
Case Report: A 49 year old African American male with past medical history of hypertension, diabetes
and anemia presented with one day of acute onset abdominal pain that woke him from sleep. Patient
denied any preceding trauma or associated nausea, vomiting or diarrhea. He had visited the emergency
department one month before for medication refills, and had been diagnosed incidentally with
normocytic anemia (hemoglobin of 8.5 gm/dL.) On physical examination, he was borderline
hypotensive; his abdomen was soft but diffusely tender with voluntary guarding. Stool was guaiac
negative. Initial hemoglobin was 6.9 gm/dL which decreased to 5.1 gm/dL hours later. Laboratory
studies were notable for hyperproteinemia with a protein gap, hypercalcemia, elevated LDH and acute
renal failure. Abdominal imaging revealed hemoperitoneum with greatest amount of blood near the
spleen, which appeared enlarged but without any active bleeding or laceration. The patient received
emergent fluid hydration and blood transfusion without adequate response in hemoglobin, and a
splenic angiogram was performed which did not reveal any active extravasation. The source of the
bleeding was thought to be secondary to a slow but persistent splenic venous bleed and the proximal
splenic artery was embolized to prevent further bleeding. Serum electrophoresis was significant for IGG
monoclonal gammopathy lambda type. A lymphoma panel of peripheral blood revealed clonal
population of plasma cells (17%) that expressed CD38, CD138 and lambda, but were negative for CD45,
CD56, CD19 and CD20 expression. Patient had elevated serum free lambda light chains. Further imaging
revealed supraclavicular lymphadenopathy and retroperitoneal and intra-abdominal lymphadenopathy
with lytic lesions in thoracic vertebral bodies. The patient was transferred to an outside specialty center
where a bone marrow biopsy revealed CD138 positive plasma cells which were about 70% of marrow
cellularity. Cytogenetic studies were significant for t(14;20) translocation, gain of long arm of
chromosome 1, loss of chromosome 13 which indicate poor prognosis.
[Date]
Discussion: PCL usually presents with signs and symptoms which are often seen in multiple myeloma
and other leukemias. It is unclear whether our patient had underlying myeloma prior to presentation
which progressed to PCL vs. primary PCL. Spontaneous splenic rupture is a rare occurrence but it has
been reported to occur in acute and chronic leukemia. Only four case reports of spontaneous splenic
ruptures have been reported with PCL, making it a rare but potentially fatal complication of an already
aggressive and deadly disease.
291
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Niktha Kasinathan, MD
Pulmonary hypertension induced by hyperthyroidism
First Author: Niktha Kasinathan M.D., Chhaya Makhija M.D.
Introduction: Hyperthyroidism is a common endocrine disorder and frequently causes cardiac
complications. Common cardiac manifestations related to hyperthyroidism are atrial dysrhythmias, sinus
tachycardia, decreased diastolic pressure, increased cardiac output, widened pulse pressure, and cardiac
failure. Isolated right heart failure, tricuspid regurgitation, and pulmonary hypertension in patients with
thyrotoxicosis have rarely been reported in literature.
Case Description: A 27-year-old male with past medical history of untreated hyperthyroidism for 3 years
presented with complaints of dyspnea, unintentional weight loss of 100 pounds, fatigue, and
palpitations. Physical examination revealed blood pressure of 163/87 mmHg, heart rate of 114
beats/minute, pulse oximetry of 97 percent on room air. A diffuse, non-tender and soft goiter with
prominent thyroid bruit was noted. Other findings were significant for presence of lid lag, mild
proptosis, jugular venous distention of 7cm, pansystolic murmur at the left sternal border,
hepatomegaly, and bilateral lower extremity edema. Electrocardiogram showed sinus tachycardia.
Laboratory evaluation revealed suppressed TSH of 0.01 uIu/ml (0.34-4.82 uIu/ml), Free T4 of 4.45 ng/dl
(0.70-1.48 ng/dl), total T3 of 181 ng/dl (58-159 ng/gl), hematocrit of 31%, and normal metabolic panel.
Presence of a large goiter with thyroid bruit, mild ophthalmopathy and substantial elevation of thyroid
receptor antibodies confirmed Graves’ disease. Treatment with methimazole and propranolol was
instituted. 2D echocardiogram showed severe pulmonary hypertension with pulmonary artery systolic
pressure of 100 mmHg, trace tricuspid regurgitation and ejection fraction of 65%. There was no
evidence of structural or valvular abnormalities. Initial work up for alternative causes of pulmonary
hypertension was negative for parenchymal lung disease, pulmonary thromboembolic disease,
hypoxemia, collagen vascular disease, HIV, drugs and toxins. Within three weeks our patient had clinical
resolution of dyspnea and lower extremity edema with diuretics and antithyroid therapy. He is
scheduled for a repeat 2D Echocardiogram and right heart catheterization once euthyroid status is
achieved to confirm the reversibility of hyperthyroidism induced pulmonary hypertension.
[Date]
Discussion: This case illustrates a rare case of pulmonary hypertension in association with severe
hyperthyroidism. Proposed mechanisms of pulmonary hypertension in such cases include high cardiac
output-induced endothelial injury, increased metabolism of intrinsic pulmonary vasodilating substances
resulting in elevated pulmonary vascular resistance, and autoimmune phenomenon associated with
endothelial dysfunction. Given it’s treatable entity, it is important to include hyperthyroidism in the
differential diagnosis of pulmonary hypertension or unexplained right heart failure.
292
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Niktha Kasinathan, MD
Hypercalcemia and rash
First Author: Niktha Kasinathan, MD, Shumaila Kashif M.D., Douglas Zaeh M.D.
Introduction: Human T-Lymphotrophic virus is a retrovirus that infects millions of people worldwide,
however it is associated with disease in only 5 percent of these individuals. One well recognized disease
association with the virus is adult T cell leukemia-lymphoma. Given the epidemiology of the virus it is
rarely encountered by physicians in North America.
Case Description: 70-year-old Haitian female previously in her usual state of health, presents with left
lower quadrant abdominal pain radiating to the flank worsening over the past 3 weeks. The pain was
associated with dysuria, frequency, and retention. She also had complaints of constipation, decreased
appetite, and chills. She denied any night sweats, change in weight, nausea, vomiting, or diarrhea.
Physical exam revealed bilateral cervical lymphadenopathy. Nodes were non-tender, fixed; ranging 1-2
cm. Skin showed an erythematous, papular, non-puritic rash covering the back and shoulders. Patient
also had suprapubic abdominal tenderness and left costovertebral angle tenderness.
Labs on admission were significant for calcium of 16.34, ALP 218, white count of 14.5 with 31%
lymphocytes including atypical lymphocytes, 20% smudge cells, and 4% bands. Hemoglobin 11.1,
hematocrit 34.1, and platelet count of 241. Electrolytes were significant for a BUN of 24 and creatinine
of 1.4.
CT abdomen and pelvis, obtained secondary to abdominal pain, revealed significant inguinal
lymphadenopathy suspicious for a lymphoproliferative disease, along with an 18mm non obstructing
stone in the left kidney.
Peripheral blood smear showed atypical hypernucleated lymphocytes, and ELISA was positive for HTLV1. Further work up with flow cytometry confirmed T cell lymphoma.
The diagnosis of HTLV-1 positive adult T cell lymphoma was made and patient underwent chemotherapy
treatment. She underwent 5 cycles of combination chemotherapy consisting of etoposide, prednisone,
vincristine, and chyclophosphomide. Patient is currently in remission as per her last PET scan.
[Date]
Discussion: Human T-lymphotrophic virus is prevalent in southwest Japan, Caribbean regions, South
Africa, and Sub-Saharan African countries. In the United States however, the prevalence of the virus is
0.01-0.02%, and when present is mainly seen in immigrants from endemic countries. The infection
remains dormant for 20-30 years before complications such as T-cell lymphoma present. Rapidly
progressive skin lesions, hypercalcemia, and lymphocytosis with cells containing lobulated nuclei, or
“flower cells,” dominate the clinical picture. HTLV-1 ATL is treated with combination chemotherapy
similar to other forms of lymphoma. Along with this treatment, post-chemotherapy interferon alpha and
zidovudine may extend survival.
293
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Javier A Lopez-Moncayo, MD
It’s Supposed to Give You “Wings,” Not a New Heart Valve!
First Author: Javier A Lopez-Moncayo, MD Julie Pantelick, DO
INTRODUCTION: Bicuspid aortic valve (BAV) is the mostcommon congenital cardiac defect. Associated
findingsincluding dilation of the proximal ascendingaorta secondary to abnormalities of the aortic
mediaare independent of whether the valve is functionallynormal, stenotic or incompetent. Although
symptomsoften manifest in adulthood, there is a wide spectrumof presentations ranging from severe
disease detectedin utero to asymptomatic disease in old age. Because itis a disease of valve and aorta,
surgical decision makingis complicated.
CASE REPORT: A 28 year-old Hispanic male presentedto the ER with acute-onset chest pain. While at
workas a roofer, the patient drank “a Red Bull energydrink”. Within minutes the patient developed
substernalchest pain, headache, nausea and shortnessof breath. There was no prior history of
personalnor family illness. In the ER he was found to be diaphoreticand pulseless in all 4 extremities. He
washypertensive and bradycardic with a 2/4, harsh, systolicmurmur in the second intercostal space on
the 60right. Chest radiograph showed a widened mediastinum.Computerized tomography
demonstrated anascending aortic aneurysm with aortic root dissection,hemopericardium associated
with a descendingthoracic aortic aneurysm without dissection, andpolycystic kidney disease. 2Dechocardiographyconfirmed severe concentric left ventricular hypertrophy,a bicuspid aortic valve, a
severely dilated aorticroot dissection, and hemorrhagic pericardial effusion.Emergent cardio thoracic
surgery was performedfor aortic root and aortic valve replacement with reimplantationof the coronary
arteries and placementof a St. Jude mechanical valve. Pathology confirmedmyxoid medial degeneration
of the aortic root but otherwiseunremarkable valve histology. There were noimmediate post surgical
complications, but days laterthe patient reported persistent headaches. Axial computerizedtomography
revealed multiple aneurysmsin the left internal carotid artery, left posterior communicating,and right
middle cerebral trifurcation.Anticoagulation was started. Complications includeda benign hematoma at
the surgical access site.
[Date]
DISCUSSION: Consumption of energy drinks carrypotential danger. We offer insight into a patient athigh
risk of cardiovascular collapse, while promotingvalve-preserving surgeries for BAV associated
withdilatation of the aorta. Recent studies show this approachhas excellent results, including
stabilization ofthe aortic root while improving valve durability.
294
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Adaeze Nwosu Iheme, MD
Lance-Adams Syndrome: Post- hypoxic myoclonus
First Author: Adaeze Nwosu-Iheme, MD Sowmini Medavaram, MD
Chronic post-hypoxic myoclonus, also known as Lance-Adams syndrome (LAS), is a rare complication of
successful cardiopulmonary resuscitation often accompanied by action myoclonus and cerebellar ataxia
seen days-weeks after the event..Early diagnosis is crucial as adequate treatment and rehabilitation can
cause significant improvement in functional status.
37 year- old African-American female with history of hypertension and cardiomyopathy had cardiorespiratory arrest after she was admitted for increasing shortness of breath when she was 29 weeks
pregnant. Pt had return of spontaneous circulation after 2 minutes of chest compressions. Emergent Csection was done at the bedside with delivery of a live fetus .On day 1 she had a witnessed generalized
tonic-clonic seizure and was treated with phenytoin which controlled the seizures. On day 2 patient had
intentional myoclonic jerks after regaining consciousness and EEG was consistent with myoclonus. Pt
continued to have myoclonic movements of the limbs and trunk associated with aphonia, dysphagia and
blurry vision. Myoclonus was exacerbated with voluntary movement, tactile stimulation and would
disappear at rest or sleep. Pt was unable to sit from sleeping position or carry out simple, co-ordinated
manual tasks like holding a cup. As there was no improvement in her condition with phenytoin, it was
decided to switch to levetiracetam500mg twice daily. Her clinical condition significantly improved within
6 days with minimal dysarthria and her myoclonus was reduced in severity and frequency.
With the help of physical therapy on day 16 post- arrest patient was able to get out of the bed into chair
with minimal assistance and able to carry out co-ordinated activities. Pt was discharged on home
physical therapy and levetiracetam. Pt was seen in the clinic after 5 weeks and the jerks improved, but
she still had difficulty with fine motor movements.
[Date]
LAS is rare condition characterized by action myoclonus which is aggravated by intentional movements
and attenuated during sleep. The patho-physiology is related to an abnormal findings of diverse neurochemicals, in particular, loss of serotonin and GABA(gamma-amino butyric acid). Our diagnosis was
established by history of cardiac arrest, symptoms of myoclonus and MRI showing areas of acute
ischemia. Early diagnosis of LAS is important as combination of physical rehabilitation and medications
will provide significant improvement of symptoms. It is important to distinguish LAS from post hypoxic
seizures as it has a prognostic significance. The important clinical features is consciousness. In the acute
type of posthypoxic seizures, the patient's mental status persists as comatose, but in LAS, the patient
later regains consciousness. LAS develops several days after the hypoxic brain insult and persists
thereafter, but in posthypoxic seizures myoclonus usually occurs within 48 hours after CPR Combination
of clonazepam, sodium valproate and levetiracetam are effective in controlling the symptoms of LAS.
295
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Kunal Manmohan Patel, MD
Dtap-Vaccine Induced Myopericarditis Mimicking ST Elevation Myocardial
Infarction
First Author: Kunal Manmohan Patel, MD PALOMA PERALTA MD, JOAQUIM J CORREIA MD, FAYEZ
SHAMOON MD
INTRODUCTION: Vaccine related myocarditis is one rare cause of myocarditis. Smallpox vaccinationinduced myocarditis has been well-reported in literature however only two cases of myocarditis related
to DTaP vaccination have been reported. Both of these cases were documented in the pediatric
population.
CASE DESCRIPTION: We present a 37 year old Portuguese male with past medical history only significant
for drug abuse that came to the emergency room with complaints of pressure like chest pains, pleuritic
in nature associated with fevers and chills for five days. The patient had a DTAP vaccine placed five days
prior to the admission after which his symptoms began. Upon arrival to the emergency room an
electrocardiogram was performed which showed ST elevations in leads II, III , AVF , v4 and v5 . An
emergency echocardiogram done at bedside showed an ejection fraction 40% with moderate global
hypokinesis but no evidence of pericardial fluid. Immediate cardiac catheterization revealed normal
coronary arteries. First Troponin I level was elevated at 30. The patient was transferred to CCU with a
presumed differential diagnosis of Myocarditis vs Coronary Vasospasm. Rheumatologic screening and
serum viral antibody titers for suspected acute infectious causes were all negative. This included
Coxsackie virus group B, Human immunodeficiency virus (HIV), Cytomegalovirus, Ebstein-Barr virus,
Hepatitis virus family, and Influenza viruses. In addition, urine and hair samples were sent for drug
screen; they were negative for recent cocaine or amphetamine use. Cardiac MRI with and without
gadolinium was performed for definitive diagnosis and showed delayed myocardial enhancement
involving the myocardium of the mid-inferior and mid-inferolateral wall of the left ventricle. These
findings were consistent with edema, inflammation, and myocarditis. Troponin I values were trended to
monitor extent of myocardial damage and serial values reached 30, 46.4, 17.8, 0.19, respectively. The
patient was treated with Colchicine and NSAIDs and his symptoms improved significantly over the
following 3 days.
[Date]
DISCUSSION:Myocarditis has multiple etiologies however vaccine related causes are rare. In a thorough
review of literature, we found only two cases of myocarditis induced by tetanus vaccine. Both were
reported in the juvenile population: one in a 3 month old after a DTAP vaccine and the other in a 13 year
old male after tetanus vaccination. Our case may be the first one seen in an adult. DTAP induced
myocarditis should be suspected in patients with chest pains and fevers with an antecedent of the
vaccine and promptly evaluated as it can cause detrimental repercussions.
296
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Biplab K Saha, MD
Cancer related Thrombotic Microangiopathy: A deadly disease
First Author: Biplab K Saha, MD Nirav Mistry, MD Sunil Sapru, MD
Introduction: Thrombotic microangiopathy (TMA) in cancer patients is an uncommon but potentially
fatal disease. TMA differs from thrombotic thrombocytopenic purpura (TTP) or hemolytic uremic
syndrome (HUS) in clinical presentation and it is not associated with ADAMTS-13 deficiency. Survival is
weeks to months after diagnosis.
Case presentation: Fifty two year old lady with past medical history of metastatic breast cancer on
paclitaxel, came in the emergency room with the complaints of worsening lightheadedness, exertional
shortness of breath, fatigue for the past 2 weeks and bloody urine for 2 days. She denied any chest pain,
palpitation, recent weight change, cold intolerance or focal neurological symptom. The patient had
received her last dose of chemotherapy about 2 weeks back. Her vital signs revealed BP 126/52,
pulse132, respiratory rate 22, temperature 99.7 and oxygen saturation 98% on room air. Physical
examination was significant for marked conjunctival pallor and tachycardia. The rest of the examination
was normal. Laboratory data showed hemoglobin of 3.1, WBC 9.8, platelet 31000, INR 1.2, PTT 24, BUN
18, creatinine 0.8, reticulocyte 19, low haptoglobin, elevated fibrinogen, LDH 3021 and a negative
coomb’s test. Peripheral blood film showed more than 50% schistocytes in a high power field and
urinalysis was positive for large amount of blood with very few RBCs on microscopic examination. The
patient was started on corticosteroid for treatment of acute hemolytic anemia. She had received 3 units
of PRBC transfusion with repeat hemoglobin of 7.3. Subsequently, the hemoglobin dropped again to 5.3
with a platelet count of 8000.Plasmapheresis was started for thrombotic microangiopathy. The patient
received 2 cycles of plasmapheresis. Eventually, she became confused, spiked a fever and
plasmapheresis had to be stopped due to massive hemolysis.LDH at this point was 7200. Patient was
transfused with FFP but despite all efforts the patient died within a week of admission.
Discussion: Among solid tumors, TMA is most common in metastatic gastric, breast, prostate and lung
cancer. Lymphoma and Myeloma are also known to cause TMA and it may be the initial presentation of
occult malignancy. The extent of hemolysis and resultant LDH elevation are usually much worse than in
TTP or HUS. Since there is no deficiency of ADAMTS-13, this condition is usually refractory to
plasmapheresis, steroids or immunotherapy. Initiation of chemotherapy might be associated with better
outcome and survival.
[Date]
Conclusion: Although uncommon, TMA is associated with a very high mortality rate. As the clinical
course is different from other thrombotic microangiopathies and prognosis is extremely poor, early
recognition and initiation of chemotherapy, in addition to conventional management, might be
lifesaving.
297
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Aileen P Tlamsa, MD
Blood is Thicker Than Water: Early Plasmapheresis in the Treatment of Severe
Hypertriglyceridemia-Induced Pancreatitis
Aileen P Tlamsa, Jessica Riggs, Michael Yudd, RoseMarie Pasmantier, Allen Blaivas
Introduction: Severe hypertriglyceridemia (SHTG), referring to triglyceride levels >1000 mg/dL, is well
documented to be a critical condition requiring immediate intervention. SHTG has been reported to
account for approximately 10% of episodes of acute pancreatitis, the third most common cause after
gallstones and alcohol. Evidence shows that patients with SHTG suffer a higher complication rate and
disease severity during acute pancreatitis episodes. The use of plasmapheresis has been shown to be
safe and effective in rapidly lowering triglyceride levels in patients with SHTG.
Case Presentation: This is a 33 year old Hispanic man with a medical history of familial
hypertriglyceridemia, non-insulin dependent diabetes mellitus, obesity, and sleep apnea who presented
to the emergency room with a chief complaint of severe abdominal pain. The patient reported missing
his medication for 5 days prior to admission. Additionally, he reported noncompliance with diet over the
preceding two months. Upon arrival to the emergency department, the patient reported progressively
worsening abdominal pain with subsequent nausea, anorexia, and vomiting. He was found to be
tachycardic, diaphoretic and hypertensive with a low grade temperature. His abdomen was diffusely
tender with hypoactive bowel sounds. His exam was otherwise unremarkable. Serum chemistry
revealed a triglyceride level of 9,312 mg/dL with grossly lipemic blood samples. His amylase and lipase
were 342 and 375, respectively. CT of the abdomen showed nonspecific pancreatic inflammation
without necrosis. Continuous insulin infusion was initiated for enhancement of lipoprotein lipase
activity, with subcutaneous heparin and an oral fibrate for synergism in serum triglyceride reduction.
The decision was made for the patient to undergo plasmapheresis for 3 daily sessions with exchange of
4 liters plasma per session and 5% albumin replacement. After the first plasmapheresis session, the
triglyceride level dropped by 87%. Following the third session, his triglycerides remained consistently
below 500 mg/dL. The patient improved and was discharged to home in stable condition on fibrate,
statin and fish oil medications.
[Date]
Discussion: This case exemplifies the utility of rapid plasmapheresis (within 24 hours) in the
management of SHTG, particularly during episodes of acute pancreatitis. In patients with critically high
triglyceride levels, as seen in our patient, rapid reduction may not be feasible by standard interventions,
including insulin infusion, heparin, and fibrate administration. Plasmapheresis has become a viable
option in these patients. In conjunction with strict dietary and medication compliance, removal of
triglycerides from plasma has also been shown to prevent relapses of SHTG. Presently, there are no
guidelines for the use of plasmapheresis in the treatment of SHTG; however, current practices have
shown this to be a safe and effective tool.
298
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Grace Tseng, MD
Adult Patent Ductus Arteriosis in Two Siblings : Case Report and Investigation
First Author: Grace Tseng MD. 1, Asim Hussain M.D.1, Muhammad Awan M.D.1, Oleg Cheboratev M.D.2
Introduction : The ductus arteriosus is a fetal vascular connection between the main pulmonary artery
and the aorta which usually obliterates upon birth of the fetus. A patent ductus arteriosus (PDA) occurs
when the DA fails to completely close within one week after birth. PDA is common in neonates, but is a
rare finding in the adult population. In addition, having a genetic association adds an even more unique
angle to this pathology.
Case Description: A 44 year old female with no medical history was referred to the cardiology clinic with
palpitations and exertional dyspnea. She stated that she has been dsypneic since child-hood with poor
exercise tolerance. Her symptoms have worsened in the past 6 months. Her initial electrocardiogram
shows normal sinus rhythm with right axis deviation and ischemic pattern in anterior leads. A TTE
showed increased right ventricular volume and diastolic pressure. A TEE confirmed pulmonary
hypertension with a communication between the right and left pulmonary artery and descending aorta
consistent with a patent ductus arteriosus.
Her elderly sister, who has a history of hypertension, presented to the medical clinic complaining of
chest pain. Upon physical exam, a loud 4/6 pan-systolic machinery like murmur was appreciated. A
suspicion of PDA was raised. A few weeks later, the patient presented to the ER for acute chest pain and
exertional dyspnea. Her cardiac enzymes and EKG ruled out acute coronary syndrome. Subsequent 2D
echo and TEE were inconclusive. The following CT angiogram of the chest revealed a 8mm caliber artery
connection between left main pulmonary artery to the proximal descending thoracic aorta, consistent
with a PDA.
[Date]
Discussion: There has been an increase in the incidence of PDA secondary to the survival rate of preterm
infants. Nonetheless the un-repaired patent ductus arteriosus in the adult is rare in developed countries
The case also highlights a complication of the disease if it persists until adulthood; namely that the
patient may not be a candidate for repair. In addition, this abstract highlighting a PDA in two siblings
may suggest a genetic link in the family which has not been identified yet. Previous studies have
suggested that genetic abnormalities in chromosome six may predispose individuals to PDA among
other clinical features.
299
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Naveen Yellappa, MD
HOOK(ah)ED Up Pneumocytes
First Author: Naveen Yellappa, MD Second Author: Inam Khan, MD
Introduction: Idiopathic Acute Eosinophilic Pneumonia (AEP) is a rare disease which causes acute
respiratory failure and is characterized by eosinophilic infiltrates of pulmonary parenchyma. Actual
cause of this has remained a mystery with some investigators suggesting an acute hypersensitivity
reaction to an unidentified inhaled antigen in an otherwise healthy individual. Various exposures have
been associated including smoke, dust and sand. Several case reports have found temporal association
between new smokers and AEP. Here we describe an unusual presentation of AEP in a patient with
recent exposure to hookah smoking.
Case Report: 21 year old male with no significant past medical history presented to a health care facility
with 3 day history of fevers, chills, pleuritic chest pain, fatigue and worsening shortness of breath. On
admission patient was found to be hypoxic and started on 100% NRBR and empiric antibiotics. As part of
his work-up he underwent a chest CT which revealed he had patchy bilateral ground glass opacities. Due
to concern of worsening clinical status and possible transition to ARDS, patient was transferred to our
center for higher level of care. On arrival to our hospital, patient was immediately intubated for hypoxic
respiratory failure. As part of the work-up, he underwent a bronchoscopy which revealed >25%
eosinophils in sputum. Patient was started on high dose steroids, 1gm per day for 3 days. His overall
condition improved steadily and he was extubated within a week and transferred out of the unit. He was
discharged home within the next few days. On further questioning the patient, once his medical status
improved, it was revealed that he had been experimenting with smoking for the last few months and
had recently been frequenting hookah bars with friends and most recently about 2-3 days prior to him
falling sick.
[Date]
Discussion: AEP typically occurs in men in the age group of 20-40. They present as n acute febrile illness
with malaise, myalgia, night sweats and pleuritic chest pain. Hypoxic respiratory failure is frequently
identified at presentation requiring mechanical ventilation. CT chest findings show bilateral patchy
ground glass opacities. Analysis of BAL specimen shows high number of eosinophils (>25%). Diagnosis is
based on these factors. Biopsy is done if diagnosis is unclear. Our patient met all the above mentioned
criteria and he responded appropriately to the treatment with high dose steroids. The teaching point
related to this case is the temporal association with hookah smoking. A few cases have been reported,
mostly abroad regarding this association. A rare albeit important association with youngsters
frequenting hookah bars more often; this is a differential we need to consider when patients present
with hypoxic respiratory failure.
300
NEW JERSEY POSTER FINALIST - CLINICAL VIGNETTE Ping Zhang, MD
STATIN AND ACQUIRED VITAMIN B12 DEFICIENCY
Ping Zhang, MD, Nilma Malik, MD Qiang Nai, MD Abdalla Yousif, MD, Raritan Bay Medical Center
(Abdalla M Yousif, MD, FACP)
INTRODUCTION: Vitamin B12 deficiency is estimated to affect 10%-15% of people over the age of 60.
Besides malabsorption and pernicious anemia, prolonged usage of certain medications have been linked
with Vitamin B12 deficiency.
CASE PRESENTATION: 65 year old female patient with PMHx of HTN and hyperlipidemia presented to
ER for one syncope episode. She denied head trauma, no headache, no vision or hearing changes, no
palpitation, no weakness or numbness, no abdominal discomfort, no diarrhea or weight loss. She eats
balanced diet all her life and she was on HCTZ-candesartan and atenolol for hypertension, and
pravastatin was started for hyperlipidemia 10 months ago. Upon admission, her vitals were HR 70, BP
106/53, RR 16, O2 saturation 100% on room air, temperature 99.0. Physical examination including
neurological examination was within normal limits. Lab values: Hb 13 g/dl, and MCV 103 fl, compared to
Hb 14.2 g/dl and MCV 90.2 fl 10 months ago, Vitamin B12 88 pg/ml, and folic acid was 17.1 ng/ml,
homocystine was 27.9 µmol/L, and methylmalonic acid was 1541 nmol/l. Further investigation including
MRI, carotid ultrasound, electrolytes and EEG were re-assuring. Vitamin B12 deficiency was diagnosed
and pt was prescribed with PO Vitamin B12 and discharged home.
[Date]
DISCUSSION: Prevalence of vitamin deficiencies increases with age. Prolonged usage of medications
such as metformin and H2 blocker have been shown to associated with Vitamin B12 deficiency. One
previous study has shown a correlation of simvastatin with vitamin B12 deficiency. In the past, screening
for vitamin B-12 deficiency was indicated only for the evaluation of those with relevant symptoms and
signs, such as anemia, neuropathy, or cognitive impairment. However, elderly people who have Vitamin
B12 deficiency frequently lack the classical signs and symptoms. Statins are widely prescribe as a long
term therapy for hyperlipidemia and our case and other studies have shown possible correlations of
acquired Vitamin B12 deficiency with chronic statins’ usage. Therefore, it seems reasonable to draw
baseline CBC and/or Vitamin B12 level and monitor vitamin B12 levels periodically in patients taking
stains.
301
NEW MEXICO POSTER FINALIST - CLINICAL VIGNETTE Alberto Aguayo-Rico, MD
A close encounter of the mixed kind
Alberto Aguayo-Rico MD Patrick Rendon MD
HIV is known for its extensive manifestations varying from immunodeficiency, inflammatory
consequences, opportunistic infections and malignancies. However, other presentations have been
described in the literature, such as those related to anemia, which in-and-of-itself can vary in the type of
anemia affecting patients with HIV.
A 64-year-old man with PMH of HTN presented to the ED with initial complaints of dizziness and a
syncopal episode. At that time he was baking near a hot oven when he had a witnessed syncopal
episode lasting 2 minutes with no seizure activity or postictal state. He was evaluated for cardiac
etiologies, and at that time diagnosed with vasovagal syncope. Ten days later he presented again with
three days of progressive dyspnea. In addition, he noted a history of worsening fatigue and a 30 pound
unintentional weight loss over the past year.
On physical exam his vital signs were normal. A mildly enlarged, soft, freely-movable lymph node was
noted on the left cervical area. His labs were significant for a hemoglobin of 6.7 from 14.3 ten days
earlier. Haptoglobin was low with an elevated LDH. Testing was positive for Coombs, IgG and
complement; and the peripheral smear revealed red blood cell agglutination suggesting a mixed cold
and warm autoimmune hemolytic anemia. Additional testing revealed a new diagnosis of HIV. An
excisional biopsy was obtained on an axillary lymph node to rule out lymphoma. The biopsy results
indicated a reactive lymph node with follicular hyperplasia.
The patient was diagnosed with a mixed warm and cold agglutinin autoimmune hemolytic anemia
(mixed-type AIHA) secondary to HIV. He was started on 1 mg/kg of prednisone, HARRT for his HIV as
well as IM Penicillin for late latent syphilis prior to discharge. He was scheduled for a follow-up in HIV
clinic and was without symptoms at the time of discharge. On further follow up visits with hematology
his hemoglobin significantly improved and he has remained asymptomatic since that time.
[Date]
In patients with AIDS, it is known that a positive Coomb’s test can be present in up to 43% of these
patients; however overt hemolysis occurs infrequently. Our case demonstrates a very rare manifestation
of mixed-AIHA in HIV, its evaluation and management. This case also demonstrates that not all HIVrelated manifestations of anemia are straight forward, with this particular case demonstrating an upfront view, the most extreme case of a ‘close encounter of the mixed kind.’
302
NEW MEXICO POSTER FINALIST - CLINICAL VIGNETTE Christopher D Bailey, DO
Eyes Wide Shut: An Uncommon Presentation of Recurrent Granulomatosis with
Polyangiitis
Christopher Bailey, DO, Shannon Jenkins, MS-IV, Peggy Beeley, MD
Introduction: Granulomatosis with polyangiitis (GPA), also known as Wegener’s granulomatosis, is a rare
disease characterized by a systemic necrotizing small-vessel vasculitis of unknown origin. It typically
affects the upper respiratory tract, lungs, and kidneys, but any organ can be affected. This case presents
a particularly unusual presentation of GPA.
Description: The patient was a 22-year-old Caucasian female with ANCA-positive GPA. She complained of
fever, chills, nausea, vomiting, and severe headache for two weeks. Additionally, she had severe eye
pain for one month along with blurry vision and double vision for two months. Her fiancée had noted
drooping eyelids and bulging of her eyes, and that she required assistance with most activities of daily
living, for one month. Vital signs were normal. Physical exam was notable for bilateral proptosis, severe
upper lid ptosis, dilated and fixed pupils, right-sided trochlear palsy, partial right and complete left
paralysis of the abducens nerve, and altered mental status. Her visual acuity was significantly reduced.
Laboratory studies were notable for elevated ESR and CRP. LH, TSH, FT4, FT3 and total T3 were
diminished. Lactate and ANCA levels were normal. A head CT scan showed a large suprasellar mass, and
an MRI of the head showed leptomeningeal involvement.
On hospital day two, She developed anisocoria and was transferred to the neurosurgery intensive care
unit. She also had hypernatremia secondary to diabetes insipidus. She began cyclophosphamide and
steroid therapy. During her 31-day hospital course, she showed dramatic improvement in her vision and
extraocular movement. With clinical improvement and regression of the mass, the neurosurgery team
declined to perform a biopsy. There was no evidence of recurrence at on follow-up four weeks later.
Discussion: GPA is a rare disease that can affect all organ systems, leading to significant variation in
presentation. This patient showed a classic clinical presentation of granulomatous hypophysitis,
displaying hypopituitarism, diabetes insipidus, and visual disturbances. This is very rare, with an
incidence of one case per 10 million per year. Based on the patient’s chronic underlying diagnosis,
negative infectious workup, and successful response to steroid therapy, granulomatous hypophysitis
secondary to GPA remains the most likely diagnosis without the tissue biopsy necessary for a definitive
diagnosis. Current medical management is cyclophosphamide and steroid therapy, which is associated
with a 50% decreased chance of relapse as opposed to steroid therapy alone. This patient underwent
this therapy with good initial outcome and avoided surgical intervention.
[Date]
This case represents a unique manifestation of GPA known as granulomatous hypophysitis. Prompt
medical management is important for favorable clinical outcomes. The dramatic improvement in clinical
symptoms and follow-up imaging, along with no evidence of recurrence on follow-up, justify our
management.
303
NEW MEXICO POSTER FINALIST - CLINICAL VIGNETTE Kristen M Gonzales, MD
Biopsy-Confirmed Renal Injury in a Case of Levamisole-Induced ANCA Vasculitis
First Author: Kristen M Gonzales, MD Second Author: Benjamin Deaton MD Third Author: Thomas
Vander Jagt, MSIV Fourth Author: Jennifer Jernigan MD
Background: Levamisole is a common adulterant of cocaine and has been isolated in approximately 80%
of the U.S cocaine supply. Initially used as a chemotherapeutic agent, levamisole has
immunomodulatory effects and a severe side effect profile. It is associated with a clinical syndrome of
cutaneous purpuric lesions, arthralgias, leukopenia, and ANCA-positivity. However, the spectrum of
systemic disease is widespread and can include renal manifestations, of which there is a paucity of data,
and only one kidney biopsy has been reported to date. We present a case of biopsy-proven pauciimmune glomerulonephritis in an active cocaine user with the vasculitic syndrome of levamisole toxicity.
Case Report: A 65-year-old man with hepatitis C virus, type 2 diabetes, and active cocaine abuse
presented to the Emergency Department with non-healing skin lesions. His last cocaine ingestion was
reportedly 2 weeks prior. His creatinine was 3.42 mg/dL at presentation (baseline 0.9mg/dL 2 years
prior). ESR was 111 mm/hr and CRP was 1.6 mg/dL. ANA titer was 1:320, p-ANCA titer was 1:10240, and
anti-MPO was elevated. Skin lesions were most notable in bilateral upper and lower extremities, trunk,
upper back, and bilateral ear lobes. Biopsies of 2 sites revealed thrombotic vasculopathy consistent with
levamisole-induced vasculitis.
Given concern for vasculitis and possible contribution from diabetes mellitus, a renal biopsy was
performed revealing focal endocapillary, pauci-immune glomerulonephritis. Features of
cryoglobulinemic glomerulonephritis were not identified. Creatinine remained elevated after discharge
between 3-3.7 mg/dL and GFR <30, suggesting CKD.
Discussion: Levamisole has been reported to potentiate the stimulant effects of cocaine, acting
synergistically and additively on acetylcholine and dopaminergic receptors. Its immunomodulatory
effects result in an ANCA-positive syndrome characterized by autoantibody formation leading to diffuse
vasculopathy and a variety of systemic manifestations. Of these manifestations levamisole-induced
renal dysfunction is an emerging entity which remains poorly described.
[Date]
One report published in April 2014 recognized a patient with likely, although not biopsy-proven, AKI
secondary to levamisole toxicity. Prior to this there was a report of levamisole-induced nephrotic
syndrome, but confirmatory renal biopsy was lacking. The only documented biopsy-proven case of
pauci-immune focal glomerulonephritis associated with levamisole-adulterated cocaine was published in
2011, and there has been limited data since. Our case is unique in that both skin and renal biopsies
were performed, both of which demonstrated histological consistency with an underlying levamisolemediated process. Thus, this report highlights the need for practitioners to be cognizant of levamisoleadulterated cocaine as a potential cause of both AKI and CKD in select patient groups presenting with
other classical findings of levamisole toxicity.
304
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Gyanendra K Acharya, MD
Fatal Non-Hepatic Hyperammonemia in ICU Setting – A Rare but Serious
Complication following Bariatric Surgery
First Author: Gyanendra K Acharya MD. Harmanjot Kaur MD. Sunil Mehra MD
INTRODUCTION: Bariatric surgery is well established in reducing weight and improving the obesity
associated morbidity and mortality. Neurological complications such as hyperammonemic
encephalopathy following bariatric surgery are rare but highly fatal if it is not diagnosed and managed
aggressively in time. Both macro and micro-nutrients deficiencies seem to play role in unmasking the
functional deficiency of urea cycle enzymes in an adult woman after bariatric surgery.
CASE PRESENTATION: 42 years old Hispanic female with past history of chronic abdominal pain, Protein
Energy Malnutrition (PEM) and Roux-en-Y Gastric Bypass Procedure (RYGBP) for morbid obesity was
brought to ER because she was found unconscious. On Physical, patient remained unresponsive to
verbal commands. Systemic exam revealed ascites and B/L pedal edema. Vitals were stable with pulse
oxygen 97%. Initial labs CBC/Serum Glucose/Urine Analysis/Arterial Blood Gas were unremarkable;
however urinary toxicology was positive for poly-pharmacy. Patient was empirically treated with Narcan
and Flumazenil but patient did not improve and remained obtunded. The patient was intubated. Further
investigations revealed serum Ammonia (193 umol/l), INR (2.01), albumin (1.5 gm/l), low pre-albumin,
normal liver enzymes, mild hepatomegaly with steatosis on CT abdomen and normal CT head. With IV
fluid, oral lactulose and rifaximin over 24 hrs, clinical status and ammonia level (127 umol/l) improved
and she was extubated next day. Blood lab revealed immune/viral Hepatitis panel-negative; Vitamin
B12/folate level-normal; valproate/lithium level- negative and low Zinc level. Despite optimum
treatment for Hyperammonemia, patient’s clinical condition deteriorated and she was re-intubated.
Ammonia levels fluctuated with peak level at 491umol/l. At this stage, we considered alternative causes
of Hyperammonemia and conducted plasma amino acid profile and urinary orotic acid levels. With
elevated Urinary orotic acid and serum ornithine, Normal/low-normal serum arginine and citruline along
with other findings, we concluded that non-hepatic Hyperammonemia may result from unmasking of
functional deficiency of urea cycle enzymes in a malnourished woman following bariatric surgery. With
rapid deterioration to coma, cerebral edema, Status Epilepticus, multisystem organ failure and death, no
confirmatory enzymes assay and DNA testing were done.
[Date]
DISCUSSION: Hyperammonemia Encephalopathy following bariatric surgery in the context of normal
liver function tests becomes diagnostically challenging for physicians. The exact mechanism of
Hyperammonemia in such patient is still not clear but more data are gradually emerging in the support
of causal-effect relationship among the triad of Hyperammonemia, nutritional complications following
bariatric surgery and functional deficiency of urea cycle enzymes. We emphasize the importance to
consider secondary causes of Hyperammonemia if conventional treatment methods does not responds
in an adult woman after bariatric surgery.
305
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Ashwad Afzal, MD
Unmasking Autoimmune Pancreatitis from Pancreatic Cancer
First Author: Ashwad Afzal Second Author: Seema Chittalae, Paloma Alejandro, Petros Efthimiou
Introduction: Autoimmune Pancreatitis (AIP) is difficult to distinguish from pancreatic cancer. Pancreatic
cancer has an insidious onset with anorexia, nausea, vomiting, loss of appetite, mid-epigastric pain and
significant weight loss. AIP also has a similar clinical presentation and is one component of a systemic
disease, IgG4 related sclerosing disease. IgG4 related sclerosing disease is characterized by extensive
IgG4 positive plasma cells and T-lymphocytes which may involve the pancreas, bile duct, retroperitoneum, salivary glands and other organs.
Case presentation: A 76 year old male, legally blind with past medical history of Hypertension,
Hyperlipidemia, Coronary Artery Disease with stents, Diabetes Mellitus Type 2 (established for 25 years)
presented with nausea, vomiting, appetite loss associated and 39 lbs weight loss over 3 months. His is
an ex-smoker with 30 pack year history. No significant surgical and family history. Vitals signs were
stable. BMI was 24.91kg/m2. Pertinent physical exam findings were no sclera icterus, no
lymphadenopathy, normal bowel sounds with tenderness to palpation over epigastric area. Routine
bloodwork including complete blood count, renal and liver function tests were normal. An Endoscopic
Ultrasound showed a 3 by 2 cm mass on the tail of the pancreas with no lymph node involvement.
Patient underwent successful distal pancreactectomy and splenectomy with no post-operative
complications. Surgical pathology report of the spleen and distal pancreas detected no carcinoma.
Microscopic Examination revealed dense lymphoplasmacytic infiltrate with onion-skin pattern fibrosis
and lobular atrophy in the medium sized pancreatic duct, consistent with lymphoplasmacytic sclerosing
pancreatitis. Immunohistochemical staining shows 30-40 IgG4 positive plasma cells/HPF and further labs
revealed igG4 level of 272.5md/dl consistent with the diagnosis of AIP.
[Date]
Conclusion: Autoimmune pancreatitis is a difficult diagnosis to attain as the presentation is very similar
to pancreatic cancer. The diagnosis is based on clinical suspicion with laboratory markers and imaging
that may help aid in the diagnosis. However, laboratory markers may be normal and a biopsy is required
to make the diagnosis. Failure to differentiate autoimmune pancreatitis from pancreatic cancer can lead
to unnecessary resection of the pancreas along with complications of surgery as autoimmune
pancreatitis responds well to steroid therapy. We recommend patients with pancreatic mass should be
evaluated for autoimmune pancreatitis to avoid invasive treatment.
306
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Ayobami T Akenroye, MBChB MPH
Hemophagocytic lymphohistiocytosis (HLH): The Mimicker
First Author: Ayobami T Akenroye, MBChB MPH Second: Nidhi Madan, MD Third: Jason Leider, MD PhD
Senior Author: Iuliana Shapira, MD
Introduction: Hemophagocytic lymphohistiocytosis (HLH), a rare but potentially fatal disease, is
characterized by excessive immune activation and cytokine release which stimulates bone marrow (BM)
macrophages to engulf hematopoietic cells. HLH is usually seen in patients with immune dysregulation
such as immunodeficiencies, hematological malignancies or autoimmune diseases. We present an AIDS
patient with HLH who presented with prolonged fever.
Case: A 45 yr old recently immigrated West African lady with AIDS (diagnosed at 32, currently on HAARTDolutegravir, Tenofovir, Emtricitabine , CD4 nadir: 170, peak viral load 20,000. Latest CD4- 218, viral
load <20copies/ml) presented with extreme fatigue, fever and chills of 2 weeks duration. Vitals: T 102.8F
HR 125/min BP 97/65mmHg. Hb: 8.9g/dl, WBC: 1.4K/µL, platelet: 126,000/µL, lactate: 2.67mmol/L,
ferritin: 16,926µg/L, LDH: 564U/L, AST/ALT: 148/24U/L, ALP: 238U/L. She was rehydrated with
intravenous fluids and given empiric antibiotics. Serial cultures remained negative. She, however,
continued to spike fevers. PPD, histoplasma, cryptococcal, Parvovirus B19, EBV, malaria & babesia
testing were negative. G-6PD activity was normal. CT-scan showed splenomegaly and retroperitoneal
lymphadenopathy. Given the lack of response to treatment, she had a BM biopsy which revealed
scattered histiocytes containing erythroid and myeloid elements and high iron storage with no evidence
of malignancy, findings consistent with HLH. Treatment with etoposide, cyclosporine and
dexamethasone was started. Within the first 2 weeks of treatment, her ferritin level fell to 5057. Her
leukopenia and thrombocytopenia initially worsened (nadir: 0.2k/µL, 10,000/µL respectively) but
improved to 2.8K and 61,000/µL. She improved and became afebrile. She was discharged to complete
chemotherapy as an outpatient. Platelet improved to 126,000/µL & WBC to 8.4K/µL. Her ferritin level
continued to decline to 1436 currently.
[Date]
Discussion: Cytotoxic T-cell activation with hypercytokinemia, which is protective in HIV/AIDS and
hinders viral replication, is responsible for macrophage activation and pancytopenia in HLH. Patients
with HIV/AIDS and HLH share various non-specific symptoms, such as fever, acute liver failure, and
splenomegaly. Consequently, identification of HLH as the cause of fever in a HIV patient could pose a
diagnostic challenge. Furthermore, fever in a patient with HIV/AIDS could be secondary to a wide range
of conditions and further contributes to this challenge. Since early suspicion and diagnosis of HLH are
critical to prompt therapy and prevention of fatality, HLH should be considered as a possible cause of
fever in AIDS patients. In this patient, as is usually the case in most patients with HLH, the initial concern
was sepsis as she met SIRS criteria. HLH should be suspected when SIRS criteria is met in a patient with
immune dysregulation, in the absence of an identified infective cause and in the presence of markedly
elevated ferritin.
307
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Hadeel Alkhairw, MD
Neurocysticercosis Presenting With Episodic Headaches
First Author: Hadeel Alkhairw, MD other authors: Anil Kapoor MD, Karen Beekman MD, Ritu Vyas MD
Headaches are often described in patients with neurocysticercosis.. Headaches may result from
increased intracranial pressure, hydrocephalus or giant subarachnoid cyst. Migraine and tension
headaches (primary type) are also more prevalent in patients with neurocysticercosis, although the
pathophysiological link is not clearly understood.
A 44 year-old Hispanic male presented with a 5 year history of recurrent headache. The headaches
were described as throbbing in the frontal area, 30 minutes to 12 hours in duration, preceded by
visualization of black horizontal lines and spots. No nausea, phonophobia, photophobia, or seizures. No
precipitating factors identified, attacks were partially alleviated by acetaminophen. Over the past few
months, headaches were noted to increase in frequency and severity affecting daily activity and
employment. Patient immigrated from Ecuador 3 years prior and denied smoking or alcohol abuse.
Vital signs and general physical examination were normal. Neurological examination was non-focal,
including cranial nerve, motor, and sensory examination. There was no sinus tenderness or
temporomandibular joint tenderness. Ophthalmological examination was normal. CT scan of the head
performed to exclude secondary causes of headache revealed multiple parenchymal calcifications in the
right occipital lobe, left frontal lobe and midline superior to the corpus callosum. Soft tissue density
measuring 6 x 9 x 13 mm was seen in the suprasellar cistern, left of midline. Magnetic Resonance
Imaging showed mid- to high intensity ring enhancement of lesions, suggestive of granular-nodular
stage of neurocysticercosis. Complete metabolic panel and blood count were normal.Serum was
positive for Cysticercosis antibody. Pituitary hormones were normal. The patient was successfully
treated with Albendazole and Prednisone. Intraparenchymal neurocysticercosis is known to present
with various neurological symptoms depending on the number, size and location of lesions.
Seizure by far is the most common presentation. Migraine has been described in the setting of chronic
inflammatory diseases like multiple sclerosis. We propose that parasitic antigen may be the source of
intermittent chronic inflammation that can trigger the trigeminal visceral nociceptive afferents
innervating the meninges and their relay in the brain stem. The locations of the lesions in the occipital
area may explain the aura. It is not clear if this condition is more prevalent in patients who are
genetically predisposed to migraine. We are not able to explain the effect of the lesion in the suprasellar
area in view of normal hormonal testing, although we cannot predict the patient will not have
endocrinologic complications in the long term.
[Date]
Our case suggests that neurocysticercosis may present with episodic migraine-like headache.
308
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Erik W Anderson, MD
RS3PE AND THE NEED FOR CANCER WORKUP
First Author: Erik Anderson, MD (ACP member) Asha Patnaik, MD Heidi Roppelt, MD Stony Brook
University
Introduction: Remitting seronegative symmetrical synovitis with pitting edema (RS3PE) is a rare
inflammatory arthritis that was first described in 1985. Since that time, there have been several case
reports describing its association with malignancy. Recognition of this syndrome is imperative since it
has an associated malignancy rate reported as high as 54%.
Case Description: A 65-year-old African-American man with a remote history of colonic adenocarcinoma
(stage II, status-post chemotherapy and resection in 1993) presented to the ER with a 6-week history of
bilateral hand swelling and pain. He described an 11-kilogram involuntary weight loss over that period.
On physical exam, there was diffuse pitting edema and tenderness to palpation of both hands.
Laboratory results were significant for a negative rheumatoid factor (RF) and anti-nuclear antibody, and
mildly elevated acute phase reactants. X-rays did not show erosive changes. A diagnosis of RS3PE was
considered and treatment with 30 mg of daily oral prednisone yielded some improvement. Computed
tomography of the chest/abdomen/pelvis was negative for mass or lymphadenopathy. Upon hospital
discharge, the patient had an incomplete response to 3 weeks of prednisone. A colonoscopy performed
5 months later revealed a large polyp (3.3 cm) in the hepatic flexure and a small sigmoid polyp, both
negative for carcinoma. The patient subsequently underwent a right hemicolectomy given the high risk
of cancer recurrence in the large polyp.
Discussion: By exclusion, this patient was diagnosed with RS3PE, a syndrome characterized by bilateral
pitting edema of the hands, sudden onset of polyarthritis, age greater than 50, and seronegativity for
RF. Seronegative rheumatoid arthritis is an important diagnostic alternative that should be considered. A
proposed mechanism for the pathogenesis of RS3PE involves increased production of vascular
endothelial growth factor and/or cytokine (IL-6), influenced by tumor cells. Glucocorticoids are the
mainstay of therapy; tocilizumab, a novel IL-6 inhibitor, has been shown in small studies to be an
effective treatment for RS3PE in cases refractory to glucocorticoid therapy.
The majority of RS3PE cases have occurred prior to or concurrent with a cancer diagnosis. There are two
case reports of RS3PE occurring subsequent to the initial cancer diagnosis; however, these patients had
active cancer at the time of diagnosis. Our case is unique in that the diagnosis of RS3PE was made 20
years after the cancer diagnosis, in the absence of active or recurrent cancer. Also, the majority of RS3PE
cases described thus far have associated concurrent malignancy with suboptimal steroid response;
however, in this case concurrent malignancy was not present, despite a suboptimal clinical response to
steroids.
[Date]
In conclusion, RS3PE is associated with multiple cancers, but may also present years after malignancy or
in the absence of active cancer. However, all patients who present with RS3PE should have an
appropriate evaluation for malignancy.
309
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Erik W Anderson, MD
OBSTRUCTIVE UROPATHY DUE TO A URETEROINGUINAL HERNIA
First Author: Erik Anderson, MD (ACP Member) Stony Brook University
Introduction: Obstructive uropathy caused by hernia-associated incarceration of the ureter is rare. When
present, the majority of cases are associated with inguinal hernias; however, incarceration is relatively
uncommon due to the invariably large size of the hernias. Early recognition of the condition is important
in order to avoid renal failure.
Case Description: An 87-year-old male with a history of polycystic kidney disease status-post bilateral
nephrectomies and a living related donor transplant in 2001 presented with fevers and shortness of
breath. He had left lower lobe crackles and a reducible right inguinal hernia. He was diagnosed with a
lobar pneumonia and treated with intravenous antibiotics. On hospital day 3, he developed an acute
kidney injury (AKI), thought to be secondary to antibiotics versus dehydration, and was started on
intravenous fluids. He subsequently developed respiratory distress secondary to pulmonary edema, and
his renal function did not improve with fluids. An ultrasound to evaluate progressively worsening AKI
revealed moderate to severe hydronephrosis of the right transplant kidney that was new compared to a
prior computed tomography (CT) scan of the abdomen/pelvis. The CT also showed moderate
hydroureter with non-visualization of the distal aspect of the ureter, suspicious for obstruction. A CT
cystogram was performed to evaluate for obstruction and revealed marked hydronephrosis and
hydroureter, demonstrating reflux into the collecting system. It also revealed incarceration of a dilated
ureter along with the anterior portion of the bladder within a fat-containing right inguinal hernia.
Urology was consulted and the patient underwent a right nephrostomy tube placement. After relief of
the obstruction, his renal function returned to baseline level. He was scheduled for outpatient ureteral
reconstruction and right inguinal hernia repair.
Discussion: Although herniation of the ureter into an inguinal hernia and subsequent incarceration is an
extremely uncommon scenario, the present case illustrates the benefit of early recognition and
treatment. It typically presents as a mass in the groin without urinary symptoms. A recent case report
describes a patient with the left ureter present in an inguinal hernia, with associated mild left
ureterohydronephrosis, although no mention of incarceration. It appears that incarceration is especially
uncommon; however, failure to diagnose can lead to serious consequences. Incarceration of the ureter
within an inguinal hernia should be included in the differential in the setting of hydronephrosis and the
detection of a hernia on physical exam or imaging.
[Date]
The present case also illustrates that nephrostomy tube placement is an important adjuvant treatment
that allows relief of the obstruction without delay, while allowing subsequent surgical exploration under
optimal conditions. Surgical repair involves careful dissection of the ureter free of the hernia, followed
by simple reduction of the hernia into the abdomen. The surgeon must be aware of the possibility of
ureteroinguinal hernia in order to avoid ureteral injury during hernia repair, which emphasizes the
importance of recognizing the condition.
310
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Suhaib Ahmad Andrabi, MBBS
Rituximab treatment in severe warm autoimmune hemolytic anemia
First Authors: Suhaib Ahmad Andrabi,MD1 Sandipkumar Patel,MD1 John Chapin,MD
Hematology/Oncology2 1: Authors are affiliated with Wyckoff heights medical center, Brooklyn NY 2:
Author is affiliated with Weill Cornell Medical college, NY
Abstract: Autoimmune hemolytic anemia (AIHA) may have a fulminant onset with life-threatening
anemia. The data regarding treatment of AIHA are limited, and rely on expert consensus. We report a
case of a 69 year old female who was admitted to the ICU with acute respiratory failure secondary to
severe hemolytic anemia. She failed to respond to high dose corticosteroids and IVIG. After treatment
with rituximab, she recovered with resolution of hemolysis.
Case: A previously healthy 69 year old female was admitted to the hospital with progressive difficulty
breathing and generalized weakness. On examination, she was alert but in severe distress and appeared
ill. Vital signs notable for a respiratory rate of 32/min. Pallor, and icterus were present but no palpable
lymphadenopathy. Chest, cardiac, and abdominal examinations were unremarkable. CBC showed a
macrocytic normochromic anemia with hemoglobin of 4.1 g/dl and RDW of 15.1 %. Hemolysis was
confirmed with reticulocyte count of 18.3 %, haptoglobin of <8 mg/dl, indirect bilirubin of 10.2 mg/dl
and LDH of 625 IU/L. The direct anti-globulin test was positive for IgG, but negative for C3d. ANA level
was 1:80, with homogenous pattern, but anti-DNA Ab was negative, with negative complement level.
Hepatitis and parvovirus B19 immunity profile were negative. Hemoglobin electrophoresis showed no
abnormalities. Bone marrow biopsy showed a hypercellular marrow with marked erythroid hyperplasia,
but no evidence of malignancy. CT scan of abdomen and pelvis was significant for peripheral
hypodensities in spleen of uncertain significance. Treatment was started with 60 mg solumedrol every
8hours and 30g IVIG daily for 3 days, but no improvement in her hemoglobin. Rituximab, a monoclonal
antibody against CD20, was started at a dose of 375mg/m2 and given weekly for four weeks. Her
hemoglobin persistently increased after the first dose, hemolysis labs improved and she recovered over
the following six weeks. She is in complete remission approximately 10 months from her initial
presentation.
[Date]
Discussion: AIHA is a rare but potentially fatal condition. It can be primary (idiopathic) or secondary to
lymphoproliferative syndromes, autoimmune diseases, infections, and malignancies. Secondary causes
of AIHA were ruled out. The first-line therapy for warm AIHA is corticosteroids, which are effective in
70–85% of patients .For patients unresponsive or intolerant to corticosteroids, splenectomy and
rituximab are the most commonly used second-line treatments. Rituximab is highly effective, with an
overall response rate (ORR) of 83-87% and complete response (CR) rate of 54-60%. We cannot rule out
an indolent splenic lymphoma as an underlying cause, but she had no risk factors or other signs of
lymphoma. Splenic lesions,have been observed in other patients with WAHA and in mice, but it is
unclear what role they play in primary pathology, or if they represent underlying B-cell disorders or
indolent lymphomas.
311
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Leila G. Bumanglag, MD
Black Esophagus: A Case of Acute Esophageal Necrosis
First Author: Leila G. Bumanglag, MD
Introduction: Acute Esophageal Necrosis (AEN) is a rare clinical entity. It presents with upper
gastrointestinal bleeding (UGIB) and is characterized by endoscopic finding of diffuse circumferential
black mucosal discoloration involving the distal esophagus, hence the term “black esophagus.” Its
etiology is not well understood. AEN is believed to arise from a combination of ischemic insult to the
esophagus, compromised mucosal protective barriers and injury caused by backflow of gastric contents.
Case Report: A 71-year-old male was brought to the emergency department after being found on the
floor of his home. He was lethargic and confused without focal neurological signs. Vital signs were:
temperature 97.7 F, BP 168/79 mmHg, HR 67/min, RR 18/min and oxygen saturation 97% on room air.
Examination findings included icterus, dried blood on his tongue, diffuse abdominal tenderness and
maroon-colored, heme-positive stool. Laboratory tests revealed hemoglobin 10.9 g/dL, WBCs 20,300
cells/dL with 95% neutrophils, platelets 104,000/mcL, BUN 65 mg/dL, serum creatinine 3.8 mg/dL, AST
8905 IU/L, ALT 4553 IU/L, total bilirubin 5.4 mg/dL, direct bilirubin 3.1 mg/dL, alkaline phosphatase 536
IU/L, amylase 133 IU/L, lipase 828 U/L, ammonia 1228 mcg/dL (19-60), INR 4.35, lactate 4.8 mmol/L.
Blood alcohol, serum acetaminophen, serum salicylate, HIV, hepatitis, malaria smear, autoimmune
hepatitis panel and urine toxicology tests were negative. CT scan showed evidence of cholecystitis and
colitis. He was admitted with cholecystitis, acute liver failure and UGIB. Antibiotics were empirically
started. He was intubated for airway protection. Lactulose and IV Esomeprazole were given. Upper
endoscopy revealed black discoloration of the distal third of the esophagus with ulcers seen more
proximally. Active bleeding was not noted. Endoscope was not passed beyond the esophagus and biopsy
was not obtained, for the risk of perforation. Liver function tests, amylase, lipase, ammonia and
leukocytosis gradually improved. On the 7th hospital day, he was extubated. Oral feeding was slowly
advanced. He denied taking any corrosive substances prior to hospitalization. On the 16th hospital day,
repeat endoscopy showed a normal esophagus and a non-bleeding ulcer on the duodenal bulb. Patient
was eventually discharged.
[Date]
Discussion: AEN, first described in 1990, is associated with male gender, older age, diabetes mellitus,
hematologic and solid organ malignancy, malnutrition, renal insufficiency, cardiovascular compromise,
trauma and thromboembolic phenomena. Multi-organ failure due to sepsis precipitated AEN in our
patient. AEN typically presents as UGIB. Biopsy is recommended, but not required for diagnosis.
Treatment is mainly supportive and management of co-morbidities. Complications include perforation,
esophageal stenosis and stricture, infection and death. Physicians should be aware of AEN as a cause of
upper UGIB in critically ill patients.
312
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Leila G. Bumanglag, MD
Superior Mesenteric Artery Syndrome: A rare cause of small bowel obstruction
First Author: Leila G. Bumanglag, MD
Introduction: Superior mesenteric artery (SMA) syndrome is an unusual and rare cause of small bowel
obstruction, characterized by compression of the third portion of the duodenum due to narrowing of
the space between the superior mesenteric artery and aorta. It is primarily attributed to loss of the
intervening mesenteric fat pad. Incidence of superior mesenteric artery syndrome is reported to be 0.10.3% of total cases of small bowel obstruction. We present a case of a middle aged man with SMA
syndrome due to extreme weight loss.
Case Report: A 59-year-old male with history of schizophrenia presented with vomiting and abdominal
distention for two days. He reported unintentional weight loss of about 50 pounds over several months
due to poor appetite. He denied any history of dysphagia or odynophagia. On examination, Vitals were
stable. He was cachectic with BMI of 17. Abdominal examination showed distension with hyperactive
bowel sounds. There were no masses or lymphadenopathy. Laboratory data, including complete blood
count, biochemical profile, HIV testing, liver function, thyroid function and malignancy work-up, was
negative. CT scan of the abdomen showed markedly dilated stomach, with a transition zone in the
duodenal sweep. Esophagogastroduodenoscopy revealed no abnormality. Diagnostic laparoscopy
revealed a remarkably distended stomach and proximal duodenum. A caliber change was noted where
the superior mesenteric artery was overriding and compressing the duodenum. The distal side of the
duodenum and the jejunum were collapsed. No obvious mass lesion was identified. Patient underwent
laparotomy and duodeno-jejunal anastomosis. Patient had uneventful post-operative recovery.
Discussion: SMA syndrome often poses a diagnostic dilemma and is considered a diagnosis of exclusion.
Most common etiology of this syndrome is significant weight loss, causing loss of mesenteric fat pad,
leading to the narrowing of the angle between the aorta and superior mesenteric artery from 38-65º to
as low as 6º, causing compression of the third part of duodenum. In the literature, anorexia nervosa, IV
drug use, HIV, gastric bypass surgery and scoliosis surgery have been associated with this syndrome.
[Date]
Delay in the diagnosis can result in malnutrition, dehydration, electrolyte abnormalities, gastric
pneumatosis, formation of an obstructing duodenal bezoar, hypovolemia, and even death. High index of
suspicion is required since clinical signs and symptoms are nonspecific. Physicians should consider the
diagnosis of SMA syndrome in patients with proximal small bowel obstruction where there is abrupt cut
off at the third portion of duodenum and imaging demonstrates an abnormality in the angle between
aorta and superior mesenteric artery.
313
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Sameer Chadha, MBBS
Anomalous Origin of Left Main Coronary Artery from Right Sinus of Valsalva
First Author: Sameer Chadha, MBBS Syed Iman Husain MD, Shikha Mehta MD, Elliot Borgen MD, Gerald
Hollander MD, Robert Frankel MD, Jacob Shani MD
Introduction: Coronary artery anomalies are rare, with an estimated prevalence of around 5% [1]. These
anomalies vary with respect to number, location, orientation of the ostia, and origin of the coronary
arteries. Some anomalies are merely anatomic variants without any clinical relevance; others can
present with chest pain, syncope, or even sudden cardiac death.
Case Presentation: A 46 year old male presented to our emergency department (ED) with complaints of
sudden onset chest pain while running for a cab. He denied any associated shortness of breath,
palpitations or dizziness. His vital signs were stable, and the results of respiratory and cardiovascular
examination were normal. An electrocardiogram performed in the ED showed ST segment elevation in
leads I, avL and V1 through V5 with reciprocal depression in the inferior leads. The patient was rushed
for an urgent cardiac catheterization which revealed narrowing at the ostium of Left Main Coronary
Artery (LMCA) that did not resolve after intra-coronary nitroglycerin was administered. However, there
was no evident atherosclerotic disease.
To better characterize the lesion, a Coronary CT Angiogram was performed, which showed that the
LMCA was anomalously originating at an acute angle from the ‘right’ coronary sinus. The CT also
highlighted the subsequent malignant course of the LMCA between proximal ascending aorta and the
pulmonary trunk. The patient was offered corrective surgical repair for this very high-risk anomaly;
however, he refused intervention despite aggressive counseling. The rest of his hospitalization was
uneventful, and he was discharged in stable condition.
Discussion: Anomalous origin of Left Main coronary artery from the Right Sinus of Valsalva (approximate
prevalence, 0.15%) is a subgroup of coronary artery anomalies that has the highest risk for clinical
repercussions. The outward expansion of the aortic root and pulmonary trunk during exertion can lead
to external compression of the LMCA which can result in acute Myocardial Infarction or Sudden Cardiac
Death [2]. The only definitive treatment is surgical repair.
Conclusion: The origin of Left Main coronary artery from the right Sinus of Valsalva is an extremely rare
coronary anomaly which can result in acute Myocardial Infarction or Sudden Cardiac Death in young
patients.
1.
Angelini P, Velasco JA, Flamm S. Coronary Anomalies: Incidence, Pathophysiology, and Clinical Relevance. Circulation 2002;
105(20):2449-54.
2.
Barth CW III, Roberts WC. Left Main Coronary Artery Originating from the Right Sinus of Valsalva and coursing between the Aorta
and Pulmonary Trunk. J Am Coll Cardiol 1986; 7(2):366-7.
[Date]
References -
314
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Christian M Chiavetta, DO
Sarcoidosis and Immune Reconstitution Inflammatory Syndrome in the Era of
Highly Active Antiretroviral Therapy
First Author: Christian M Chiavetta, DO Second Author: Priyasha Srivastava, MD Third Author: Julius
Salamera, MD
Immune Reconstitution Inflammatory Syndrome (IRIS) describes a collection of inflammatory disorders
associated with paradoxical worsening of infectious or inflammatory processes upon initiation of Highly
Active Antiretroviral Therapy (HAART). In patients with Acquired Immunodeficiency Syndrome,
worsening of pre-existing infections is seen more commonly as a manifestation of IRIS, while
autoimmune or granulomatous conditions are rare.
A case of sarcoidosis involving the lungs and gastrointestinal tract presenting as IRIS is seen rarely in
AIDS. Whether such associations represent a causal or coincidental finding is unproven. It appears that
immune reconstitution after T-Cell depletion resulting from many causes, including HIV infection, is
associated with increased susceptibility to immune dysregulation that induces Th1 immune responses
against unknown antigens that underlie granulomatous inflammation of sarcoidosis. Prior to
introduction of HAART, progressive sarcoidosis and advanced HIV infection were considered to be
divergent diseases because CD4 T cells were believed to be essential in granuloma formation. However,
the occurrence of sarcoidosis immediately following HAART, typically after >12 months, suggests that
immune reconstitution may trigger reactivation of preexisting sarcoidosis.
[Date]
A 54 year old African male was recently diagnosed with HIV and Hepatitis C virus co-infection when he
presented with progressive weight loss, anorexia, multiple pulmonary nodules, and
hepatosplenomegaly. Further testing revealed normocytic anemia, elevated alkaline phosphatase,
hypercalcemia, and transaminitis. The HIV viral load PCR was 5100720 copies/ml with a CD4 count of 56
cells/uL. Blood cultures, acid fast bacilli (AFB) blood cultures, serum cryptococcal antigen, and urine
histoplasma antigen were negative. Liver biopsy revealed non-caseating granulomata without evidence
of malignancy, and AFB and fungal cultures were negative. Bronchoscopic examination revealed no
evidence of AFB on multiple smears. He received treatment for presumed disseminated mycobacterial
infection with isoniazid, rifabutin, ethambutol, pyrazinamide, and azithromycin along with
trimethoprim-sulfa for prophylaxis against Pneumocystis jiroveci pneumonia. HAART was initiated 8
weeks after starting the above regimen. The patient was re-admitted four months later with altered
mental status, worsening hypercalcemia, acute kidney injury, mediastinal adenopathy, persistent diffuse
pulmonary nodules, and multiple splenic lesions. Intravenous fluids, corticosteroids, and calcitonin were
administered. CT-guided biopsy of splenic lesions disclosed non-caseating granulomata. Fungal as well
as AFB cultures were negative. Multiple determinations of serum angiotensin converting enzyme (ACE)
were consistently abnormal at greater than 100. Repeat CD4 count was 337 cells/uL and markedly
reduced viral load to 821 copies/ml. Hyperparathyroidism and multiple myeloma were ruled out. He
was discharged on maintenance corticosteroids with titration based on his symptomatology, serum
ionized calcium, and radiographic parameters. Outpatient follow-up showed a stable patient with
normal renal function, stable electrolytes, although he developed steroid-induced hyperglycemia.
315
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Usama Ali Daimee, MD
Abdominal Pain with Dyslipidemia: Unrelated or Something Sinister?
Usama Daimee, Scott Cameron, and Robert Block
INTRODUCTION: Cholesterol ester storage disease (CESD) is a rare lysosomal storage disorder that is
characterized by deficiency of lysosomal acid lipase and may present at different ages. The pathologic
accumulation of cholesterol esters leads to both hepatic and cardiovascular complications. We describe
a patient whose CESD diagnosis evaded physicians with treatment evolving over the course of nearly
two decades.
CASE PRESENTATION: The patient first presented at age 12 in 1989 with abdominal pain and watery
diarrhea. Her physical exam was notable for failure to thrive based on pediatric growth charts. The initial
cholesterol profile revealed total cholesterol (TC) 406, low-density lipoprotein (LDL) 356, high-density
lipoprotein (HDL) 16, and triglycerides (TG) 206. Liver enzymes at the time revealed aspartate
aminotransferase (AST) 74, alanine aminotransferase (ALT) 134, and alkaline phosphatase (ALP) 196. Her
abdominal discomfort led to extensive work-up consisting of upper and lower endoscopic biopsies,
cholescintigraphy, and stool cultures, all of which were unremarkable. Laboratory screens for several
conditions including thyroid disorder, lactase deficiency, cystic fibrosis, and autoimmune disease were
unrevealing. The patient was started on cholestyramine with a low-fat diet, which resulted in
improvement of her lipid profile.
One year later in 1990, the patient developed hepatomegaly. Right upper quadrant ultrasound showed
hyperechoic liver consistent with hepatitis. A liver biopsy led to suspicion of glycogen storage disease,
and treatment was changed to cornstarch. When her dyslipidemia worsened, cornstarch was
discontinued and cholestyramine resumed. A repeat liver biopsy in the same year, performed via wedge
resection, showed diffuse fatty change concerning for storage disease of a lipid nature. A reduced
lysosomal acid lipase (LAL) level later in 1990 established the diagnosis of CESD. She remained on
cholestyramine but was transitioned to atorvastatin by 2008. After dose adjustments and trials of
different statins, her symptoms and laboratory tests stabilized in adulthood with the combination of
atorvastatin and ezetimibe. A recent lipid panel showed TC 126, LDL 71, HDL 34, and TG 103, while
hepatic enzymes were AST 47, ALT 46, and ALP 52. Evaluation with echocardiogram, exercise tolerance
test, and carotid ultrasound over the years showed no significant abnormalities. The patient’s lipid
profile and liver enzymes are indicated graphically throughout the evolution of her treatment regimen
until symptom resolution.
[Date]
DISCUSSION: As our case illustrates, both recognition and treatment of CESD are challenging. Given its
myriad manifestations, misdiagnosis is common and a high index of suspicion is required. CESD is
identifiable through characteristic biochemical, genetic, and/or tissue findings. If detected early,
stabilization may be achieved with statins, though enzyme replacement therapy is an emerging
strategy. Close monitoring is necessary to prevent complications.
316
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Arpita Desai, MBBS
PROLONGED SURVIVAL WITHOUT SYSTEMIC CHEMOTHERAPY IN A NSCLC PATIENT
WITH PATHOLOGICALLY-CONFIRMED SKELETAL METASTASIS
First Author: Arpita Desai, MBBS
INTRODUCTION: Non-small cell lung cancer (NSCLC) is one of the most commonly occurring malignancies
and is a leading cause of cancer-related deaths worldwide. About 20 - 50% of NSCLC patients develop
metastatic disease. Oligometastases is used to describe cases of minimal distant metastasis (< 5 lesions)
that can be treated by local therapy to achieve long term survival or cure. We report a case of
oligometastatic NSCLC with skeletal metastases managed with local treatment.
CASE PRESENTATION: A 74-year-old white male, while being treated for a ruptured appendix, was
observed to have a mass in his left lung on a chest x-ray (CXR) and was treated for a presumed
pneumonia. CXR one month later showed partial improvement. However, six months later, the patient
complained of shortness of breath on strenuous activity. The physical exam and laboratory values were
unremarkable but a PET/CT scan showed a left lung density, 3.4 x 2 cm, with an intermediate SUV
uptake of 1.8. Subsequently, a CT-guided biopsy revealed adenocarcinoma. Two months later, in
October 2008, the patient underwent mediastinoscopy with biopsy and thoracoscopic left lower
lobectomy with lymph node sampling. There was no evidence of pleural or lymph node metastases, and
the bronchial margins were negative for tumor. Final diagnosis was well-differentiated adenocarcinoma
T1N0M0.
In July 2010 the patient complained of significant weight loss (about 70 lbs) and new back pain. A followup CT scan showed a new sclerotic lesion in the T11 spine. CT-guided biopsy of the lesion showed that
the sample was TTF1-positive and histologically similar to his lung primary. The patient received
palliative radiotherapy of 30Gy to the T10, T11 and T12 thoracic vertebrae. Zoledronic acid was added as
an adjunctive therapy for bone metastasis. As he did not have other evaluable sites of disease, systemic
chemotherapy was not administered. He continued to receive Zoledronic acid periodically, with CT scan
in May 2013 showing abnormal heterogeneous sclerosis diffusely involving the T11 vertebra but no
other evidence of metastatic disease.
[Date]
DISCUSSION: While studies have shown that local therapies, including radiotherapy and/or surgery, are
the preferred primary approaches in the management of oligometastatic disease, systemic therapy is
commonly employed in the general practice. Our case illustrates that long-term disease-free survival
maybe achieved following local treatment only, in patients with metachronous presentation of isolated
skeletal metastasis. This may be a feasible approach in patients with a long duration of disease free
interval prior to demonstration of oligometastatic involvement as this may portend a biologically more
indolent process.
317
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Christine A Garcia, MD
Carry Me Home: A Curious Case of Tumor-Induced Osteomalacia with Fanconi’s
Syndrome
First Author: Christine A Garcia, MD, MPH; Rishi Mehta,MD Chananya Goldman,MD; Vanya Grover, MD;
Kyung Ho Kim, MD; Nand Wadhwa, MD
Introduction: Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome characterized by
severe renal phosphate wasting due to phosphatonin-secreting mesenchymal tumors. Patients with TIO
usually present with vague, long-standing symptoms of bone and muscle pain, weakness and
osteomalacia due to severe hypophosphatemia. Occasionally, patients may present with concurrent
Fanconi’s syndrome including glucosuria, aminoaciduria and phosphaturia.
Case Description: A 34 year-old man without significant past medical history presented with 2 years of
progressively worsening lower back pain and bilateral lower extremity pain and weakness which
subsequently led to inability to walk. The patient had back pain 1 year ago without trauma and was
found to have compression fractures in the thoracic and lumbar spines on imaging. He was treated with
pain medications and did not follow up. The pain progressively worsened to bilateral upper extremity
weakness requiring complete assistance with normal activities of daily living (ADLs) including standing
up without support. He denied dysphagia, headaches, urinary and bowel incontinence. The patient lost
40 pounds and a significant amount of muscle mass. Physical exam was significant for severe temporal
wasting with profound muscle weakness in all extremities.
Discussion: Tumor-induced osteomalacia (TIO) is a rare paraneoplastic form of renal phosphate wasting
that results in severe hypophosphatemia, inappropriately low or normal 1,25OH vitamin D, and
osteomalacia. Occasionally, Fanconi syndrome accompanies the profound phosphaturia seen in TIO.
Definitive treatment is removal of the phosphatonin (usually FGF 23) secreting tumor that may
completely resolve the metabolic abnormalities. The rarity and occult nature of TIO often delays its
recognition, with average time from onset of symptoms to correct diagnosis exceeding 2.5 years and the
difficulty locating the underlying tumor adding another 5 years. This uncommon, debilitating disease
presents a formidable diagnostic challenge with protracted delay in the correct diagnosis and treatment.
Internists should consider TIO in any patient with persistent, enigmatic bone pain with renal
hypophosphatemia with or without Fanconi’s syndrome.
[Date]
The patient had severe hypophosphatemia (phosphorus level 0.9 mg/dl) with inappropriate
phosphaturia, hyperparathyroidism (PTH intact 132.6 pg/ml) with normal serum calcium, vitamin D
deficiency (25OH Vitamin D level 16) with normal 1,25-OH Vitamin D, glucosuria (with normal serum
glucose), and aminoaciduria. SPEP and UPEP were negative. CT abdomen and pelvis with intravenous
contrast showed diffuse metabolic bone disease with multiple insufficiency fractures and liver cysts with
no obvious masses. FGF-23 was elevated to 738 RU/ml [normal =180]. The patient was treated with
aggressive phosphorus, ergocalciferol and calcitriol repletions with limited improvement in muscle
strength. He was eventually discharged to subacute rehabilitation. Patient was suspected to have an
underlying occult tumor-induced osteomalacia.
318
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE NANCY GUPTA, MD,MBBS
AUTOIMMUNE HEPATITIS IN ASSOCIATION WITH SOFOSBUVIR AND RIBAVIRIN
First Author: NANCY GUPTA, MD,MBBS
Introduction. Sofosbuvir in combination with Ribavirin was approved by the Food and Drug
Administration as a treatment option for Hepatitis C (HepC) in 2013. We describe a case of autoimmune
hepatitis triggered in a patient on therapy with Sofosbuvir and Ribavirin.
Case presentation. A 65 year old woman with past medical history of diabetes mellitus, hypertension,
HepC (genotype 2) underwent pretreatment liver biopsy in May 2012 that demonstrated mild chronic
active hepatitis with focal piece meal necrosis, mild stage 1 periportal fibrosis with no increased iron
deposition. No features of autoimmune hepatitis were seen on biopsy. The patient was started on 400
mg Sofosbuvir and weight based 1000 mg Ribavirin for a planned duration of 12 weeks. Liver Function
Tests (LFTs) initially improved on therapy, however 3 weeks after the treatment initiation, patient
started complaining of weakness and fatigue. Repeat tests revealed elevated LFT’s. Autoimmune titres
were positive for anti-nuclear antibody, anti smooth muscle antibody with elevated IGG and serum
gamma globulin levels. Repeat liver biopsy in June 2014 showed markedly distorted architecture
secondary to formation of nodules completely enclosed by fibrous septa and areas of confluent necrosis
with mild to moderate chronic inflammation consisting mainly of lymphocytes and plasma cells along
with moderate to severe interface hepatitis. Balloon degeneration of hepatocytes, with rosette
formation possibly associated with regenerative activity was seen, consistent with superimposed
auoimmune hepatitis. Based on laboratory and biopsy findings, diagnosis of drug induced autoimmune
hepatitis was made and the treatment for HepC with Sofosbuvir and Ribavirin was discontinued. The
patient was subsequently started on Prednisolone with improvement in LFT’s.
Discussion. The above case describes autoimmune hepatitis after initiation of Sofosbuvir and Ribavirin.
To our knowledge, this complication has never been reported before. The most frequent adverse events
noticed with this combination regimen have been headache, anemia, fatigue, and nausea.
[Date]
The etiology for autoimmune hepatitis is unknown in most cases. It has been believed to occur in
patients with genetic susceptibility in which a trigger is required to initiate the liver injury, with
drugs/medications being a potential trigger for autoimmune hepatitis. Hepatitis C virus is usually
associated with the autoimmune diseases and it is not unreasonable to think that hepatitis C might have
triggered the autoimmune phenomenon. But in this case, the trigger was most likely the drug since the
patient had no evidence of autoimmune hepatitis until the therapy was started.
319
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Hayas Haseer Koya, MD
Unraveling The Mystery Of Neurocutaneous Manifestations In A Young Male
Hayas Haseer Koya, MD, Dona Varghese, MD, Arpan A Patel, MD, Roshni Radhakrishna, MD, Mathew Hess, MD
Introduction: The etiology of neurological symptoms with skin manifestations include a multitude of
differentials ranging from vasculitis to nutritional deficiencies. We present an unusual case of reversible
neurocutaneous manifestations in a young male.
Case Presentation: A 35 year old male with a history of pulmonary embolism (diagnosed one month prior
and on warfarin) presented with 5month history of progressive gait instability, numbness and
discoloration of hands, episodic confusion, erectile dysfunction and decreased libido. Vitals signs were
stable. Physical examination revealed hyper pigmentation of dorsum of hands and face, short term
memory deficit, psychomotor slowing, hypertonia, spasticity and hyperreflexia with ankle and patellar
clonus. A thorough infectious (including CSF analysis), vasculitis and paraneoplastic work up was
negative. Venous Doppler showed a right lower extremity DVT and INR was sub therapeutic at 1.08.
Pertinent lab results included: macrocytic anemia with hemoglobin of 11.7, MCV of108.8,
hypersegmented neutrophils on peripheral smear, normal folate, very low B12 level at 57 and
hyperhomocystenemia at 133.8. MRI revealed diffuse hyper intensity of the posterior thoracic spinal
cord from T8-T12 level consistent with sub-acute combined degeneration (SCD) of spinal cord.
Electromyography showed moderate chronic sensory motor axonal polyneuropathy. Further workup for
B12 deficiency with esophagogastroduodenoscopy(EGD) and biopsy revealed findings consistent with
autoimmune gastritis. Serologic studies revealed presence of anti-intrinsic factor antibody. A diagnosis
of encephalomyeloneuritis, SCD, and hypercoagulable state due to hyperhomocystenemia secondary to
vitamin B12 deficiency resulting from pernicious anemia was made. Patient was initially treated with
parenteral B12 and heparin followed by lifelong oral B12 supplementation and warfarin. He had
complete resolution of neurocutaneous findings in 4 weeks.
Discussion: Vitamin B12 deficiency can result in serious neurologic sequelae including dementia,
encephalopathy, ataxia, progressive weakness, and paresthesia. Rare findings include cutaneous
hyperpigmentation predominantly involving dorsum of hands and feet-the exact pathogenesis of which
is unclear but thought to be due to decreased levels of intracellular reduced glutathione(which has a
tyrosine kinase inhibitor activity) resulting from B12 deficiency, which leads to stimulation of epidermal
melanocytes and increased melanin synthesis. Clinical suspicion in the setting of pancytopenia,
hypersegmented neutrophils and neurologic symptoms should prompt measurement of cobalamin and
folate levels and if low, methylmalonate and homocystine level should be obtained. Radiological studies
show T2 hyper intensity of signals in the posterior columns of spinal cord. Work up should include
evaluation for autoantibody to intrinsic factor and an EGD. If neurological symptoms dominate
treatment includes parenteral B12 supplementation followed by lifelong oral therapy. In most of the
cases neuro-radiologic recovery occurs with supplementation of cobalamin.
[Date]
Conclusion: We reiterate the need for a careful history, physical examination and systematic work up for
diagnosis of B12 deficiency, as in most cases neurologic symptoms are reversible and resolves with B12
supplementation.
320
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Sandeep S Jubbal, MBBS
Unusual Presentation of Pulmonary Actinomycosis with 'stem-and-bud'
Appearance on CT Scan
First Author: Sandeep S Jubbal, MD Ravi R. Vinnakota, MD, Sheetal Malhotra, MD, Paul Endres, MD, Azra
Shahidi, PhD Sheldon T. Brown, MD James J Peters Veterans Affairs Medical Center
Introduction: Actinomyces is an anaerobic oral cavity commensal bacterium that can rarely
cause Actinomycosis, a disease characterized by the formation of abscesses in the oral cavity, lungs, or
gastrointestinal tract
Case: We present a case of 64 year old male chronic smoker, who presented with rash, cough and
shortness of breath. Initial CT scan chest showed no mass, but a follow up CT four months later revealed
a large, fungating, mediastinal mass leading to a diagnosis of esophageal cancer, invasive to lungs on
bronchoscopy. Subsequently, the patient underwent tumor debulking radiation and chemotherapy.
Treatment course was complicated by neutropenic fever and productive cough. Repeat CT chest
revealed extensive peripheral ‘stem-and-bud’ type infiltrates in bilateral lung fields. Fever spikes
continued despite treatment with cefepime, ampicillin, vancomycin, azithromycin, micafungin and
fluconazole. Sputum for AFB, urine legionella and serum fungal antigen assays were negative. A
bronchial lavage revealed widespread filamentous branching, beaded gram positive rods along with
polymorphs consistent with Actinomyces and “sulfa granules” were evident on cytopathology. Cultures
grew Actinomyces israelii. Review of original esophageal biopsy specimens showed squamous cell
carcinoma with concurrent Actinomycosis. A 4-week course of intravenous penicillin resulted in
suppression of fever and improvement of respiratory status.
Literature review from medical databases such as Medline, Pubmed, Ovid and others was done to look
for CT scan reports of ‘stem-and-bud’ appearance in Pulmonary Actinomycosis and presentation of
Actinomycosis. The literature review results will be presented with this case report.
Discussion: Patient had squamous cell carcinoma of the esophagus invading to the lungs with
concurrent Actinomyces infection. The infection added bulk to the tumor and later led to bronchiolar
extension due to immunosuppression from chemotherapy and radiotherapy.
[Date]
Conclusion: Actinomycosis is known to mimic solid tumors and bronchiolar extension and presents
rarely as ‘tree-and-bud’ appearance on CT as in our patient.
321
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Arunpreet S Kahlon, MBBS
LACTATEMIA OF UNKNOWN SIGNIFICANCE IN A PATIENT WITH GLIOBLASTOMA
First Author: Arunpreet S Kahlon, MBBS Amrita K. Dhillon M.B,B.S, Ganesh Aswath M.B,B.S, Najam Ud
Din MD, Jonathan Wright MD.
Introduction: Elevated lactate levels are usually seen in patients who have cellular hypoxia which can be
either due to decreased blood flow to the cells, decreased oxygen in the blood reaching the cells or
inability of the cells to utilize that oxygen. Since lactate is produced as lactic acid, it usually causes a
positive anion gap acidosis when produced in significant quantity in the body. We are presenting a rare
case of chronically elevated lactate levels in a patient with glioblastoma.
Case: A 37 year old patient with a past medical history of known glioblastoma multiforme status post
ventriculopreitoneal shunt, glucocorticoid induced diabetes, admitted for treatment of newly found
deep vein thrombosis. Except for bilateral leg swelling, patient was asymptomatic with vital signs within
normal range. On lab workup it was found that patient had an anion gap of 20, but her serum
bicarbonate levels were within normal range. Further workup revealed a plasma lactate level of 5.5
mmol/L and negative ketones. An arterial blood gas(ABG) revealed a ph- 7.40, pCO2-42mmHg, O2 sat99%, Total CO2-27mmol/L, Base excess-1 and PO2-110mmHg on 2 liters oxygen by nasal cannula. On
retrospective review of patient’s records it was found that her anion gap had been elevated for atleast 1
year. During the entire time her serum bicarbonate levels were within normal range. Serial lactate levels
and ABG revealed similar results. An MRI of brain revealed a stable tumor unchanged when compared to
prior imaging. The patient was not on any medication that could cause elevated lactate levels. She was
worked up for bacterial infections and malaria, but no infection was found.
[Date]
Discussion: Lactic acidosis has been reported in patients with highly malignant tumors. This has been
described as type B lactic acidosis. It is mainly seen in hematologic malignancies where the cell
proliferation is robust, but is rare in solid malignancies. The postulated hypothesis is ischemia of
malignant cells causing anaerobic glycolysis. Another phenomenon known as aerobic glycolysis or
Warburg effect describes lactate production in the tumor microenvironment as a selective mechanism
used by tumor cells to suppress antioncogenes and promote tumor growth factors. However this is
unlikely to cause such high lactate levels in the blood. In our patient, a thorough workup did not reveal
any obvious cause of high lactate levels for such a long duration with normal bicarbonate levels. In the
light of this we suspect that the patient’s glioblastoma may be the cause, although there is little
literature to support it. Further work needs to be done to study lactate metabolism in glioblastoma and
its significance.
322
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Morgan Samuel Kellogg, MD
Chikungunya Virus: An emerging threat? A chronical of the first American death
secondary to CHIKV
First Author: Morgan Samuel Kellogg, MD
Introduction: Chikungunya fever is caused by the Chikungunya Virus (CHIKV), transmitted primarily
by Aedes aegypti and Aedes albopictus. This year, CHIKV has become epidemic within the western
hemisphere with an epicenter in the Dominican Republic. Patients with chikungunya fever typically
experience arthralgia, fever, headache, and petechial rash. The virus is usually self-limited after several
days to weeks, and severe complications of CHIKV are infrequent. In past outbreaks, the most common
atypical manifestations of CHIKV include cardiovascular and neurological disorders. Peripheral cyanosis
has not been previously described, and notably, death secondary to CHIKV is exceedingly rare. In this
report, I present a case of the first documented death secondary to CHIKV in the U.S.
Case Presentation: A 47-year-old man with past history of alcohol abuse and pancreatitis presented to
our hospital in July, four days after traveling to the Dominican Republic where he was attending the
funeral of his sister who reportedly died of CHIKV with acute onset of progressive arthralgia and mild
headache. CHIKV and Dengue fever serology were ordered given the patient’s travel history but he was
deemed to be non-septic and supportive care at home wasrecommended.Over the subsequent days,
the patient had ongoing fever with diarrhea, one episode of syncope, progressive pain in his legs, and
developed an erythematous rash on the chest, abdomen, and back. Nine days after his return to the
U.S., he developed severe bilateral lower extremity edema prompting the patient to present back to our
ED where he was noted to be hypotensive and tachycardic. Labs revealed lactic acidosis and acute
kidneyinjury. Most strikingly, he had severe non-pitting edema of the upper and lower extremities with
dusky-blue fingertips and toes. The patient was admitted to the ICU where he experienced a progressive
course including severe shock refractory to multiple pressors, respiratory failure requiring intubation
and mechanical ventilation, gross cutaneous desquamation, renal failure requiring renal replacement,
DIC with gastrointestinal bleed, and compartment syndrome requiring fasciotomy. Two-and-a-half
weeks after admission, the patient died. The presence of CHIKV was confirmed by PCR while workup for
other etiologies including Dengue fever proved negative.
[Date]
Discussion: Given the evolving nature of the CHIKV epidemic in the Americas, American physicians can
expect to care for increasing numbers of patients with Chikungunya fever. There is ongoing work to
develop vaccines against CHIKV, but once infected, the care of patients with CHIKV remains supportive.
The optimal approach to patients with atypical or severe manifestations of CHIKV has yet to be fully
elucidated. The possibility of progressive or severe Chikungunya fever must be considered when
evaluating patients with known CHIKV or who are returning from the Caribbean or Central America.
323
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Sarah Khan, MD
Cryptococcocal Meningoencephalitis in a Non-HIV Patient - The Search for an
Underlying Disease
First Author: Sarah Khan MD, Marilou Corpuz MD
Introduction: Cryptococcal meningitis, in the absence of HIV or organ transplantation, is seen
infrequently. Other predisposing conditions for cryptococcosis include sarcoidoisis, connective tissue
disease, malignancy, glucocorticoids, and idiopathic CD4 lymphocytopenia. When patients do not have a
known underlying immune deficiency, the diagnosis of cryptococcal meningitis is a surprise that poses a
diagnostic and therapeutic dilemma, as seen in our case.
Case: An 87 yo male with a history of pulmonary embolism, deep venous thrombosis and a recent
herpes zoster infection presented with fever and worsening confusion. His wife reported that he has
been mentally declining since his zoster a few months ago. In the last few days the patient was more
confused and has been complaining of generalized pains, attributed to post herpetic neuralgia by his
private physician. On exam, the patient was intermittently confused, agitated, tachycardic and
tachypneic with a Tmax of 103. Initial lab work showed leukopenia and elevated creatinine. Lumbar
puncture showed normal pressure, CSF wbc 45 (95% lymphs), protein 114, glucose 51, positive CSF
angiotensin-converting enzyme (5.9, normal 0-2.5) and CSF crytococcal antigen of 256. Serum ACE level
was normal and serum cryptococcal antigen was 128. Patient was initially started on acyclovir for
presumed zoster encephalitis, pending CSF VZV PCR. CT thorax and abdomen pelvis was done. There
were no overt findings of pulmonary/extra pulmonary sarcoidosis or specific evidence of neoplasm. CT
showed multiple hypodensities in liver, splenomegaly with perigastric varices. CSF bacterial, viral and
fungal cultures remained negative. He was given amphotericin B lipid complex for 2 weeks, which was
changed to fluconazole. Vasculitis work up was negative. His CD4 count was 302, total T-cells of 438. His
hospital course was complicated by pneumonia, thrombophlebitis, acute kidney injury, and CHF. The
patient failed to show significant neurological improvement.
Discussion: The finding of cryptococcal meningoencephalitis in a patient without any known
predisposition to the infection is a rarity. The pursuit for the underlying problem can be monumental,
and the treatment and duration are unclear. In our patient, there are many confounding factors
including a positive CSF ACE level, but negative serum ACE and no clinical signs of sarcoidosis. A
diagnosis of idiopathic CD4 lymphocytopenia is favored in our patient. His CD4 is relatively low and he
had zoster, which has been associated with ICL patients who have cryptococcal meningitis.
Conclusion: Cryptococcal meningoencephalitis can occur in a non-HIV patient without a known
underlying immune deficiency. The diagnostic investigation can be a major undertaking.
[Date]
Idiopathic CD4 lymphopenia should be recognized in the differential diagnosis as a risk factor for
cryptococcosis.
324
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Sunyoung Lee, MD,PhD
Fulminant hepatic failure from hemophagocytic lymphohistiocytosis secondary to
hepatosplenic T-cell lymphoma
First Author: Sunyoung Lee, MD,PhD Amanda Schneier, MD, Daniel Aruch, MD, Judith Lin, MD
Case Description : A 44 year-old female with no past medical history presented for unexplained acute
jaundice and fatigue. She developed a new skin rash in the bilateral lower extremities two weeks prior,
which spread to the entire body. She received traditional Chinese herbal treatment by a Chinese
herbalist. Her rashes seemed to resolve, but she developed progressive fevers and severe jaundice over
the next two weeks. At hospital admission, she was pancytopenic with a white blood cell count (WBC)
3,800 /µL, hemoglobin 8.4 g/dL, and platelet 35,000 /mm3. Total bilirubin and direct bilirubin were 20.7
mg/dL and 18.7 mg/dL with an INR 1.4. She was admitted to the medical intensive care unit (ICU) for
acute liver failure secondary to Chinese herbal ingestion, in which she received albumin, fresh frozen
plasma, and cryoprecipitate, at one point requiring pressors for hypotention. She was treated with
vancomycin and piperacillin/tazobactam and maintained on N-acetylcysteine and prednisone. Her peak
MELD score reached 31. She remained febrile, and pancytopenia worsened. Computerized tomography
(CT) of the abdomen revealed a 4.7 cm irregular mass at the posterior right hepatic lobe. Transjugular
liver biopsy did not reach the mass, but it showed hepatocyte steatosis with portal tract fibrosis as well
as a minimal degree of hemophagocytosis interpreted as toxic liver injury with evidence of chronicity.
Due to persistent fever, progressive pancytopenia with WBC 100 /µL and unexplained RBC / platelet
transfusional requirement, bone marrow biopsy was performed, showing hypercellularity (70%) with
27% CD3+ CD52+ lymphocytes localized in sinusoids; and 73%, CD68+ histiocytes with
hemophagocytosis. A diagnosis of hemophagocytic lymphohistiocytosis (HLH) with hepatosplenic T-cell
lymphoma (HSTL) was made. With worsening bilirubin (71.2 mg/dL) and ferritin (56,856 ng/mL),
dexamethasone, pentostatin, and alemtuzumab were started. However, the patient deteriorated and
died 5 days later from cardiopulmonary arrest secondary to pneumonia.
[Date]
Discussion : This report is the first case of HTCL presenting as fulminant liver failure with secondary HLH
mimicking acute hepatotoxicity attributed to herbal ingestion. She was admitted to ICU, but the initial
treatment focus was on the management of fulminant liver failure secondary to toxic ingestion. Her
personal history, laboratory studies, and liver biopsy all supported the diagnosis. However, this delayed
the decision on bone marrow biopsy although she remained pancytopenic with unexplained fever and
very high ferritin. Later, bone marrow biopsy confirmed the diagnosis of HLH. Although abnormal liver
function is frequently seen in HLH, it is not a diagnostic criterion, and no study has been reported on
hepatic features of HLH. However, a high index of suspicion for secondary HLH is required for patients
with unexplained pancytopenia and high MELD scores.
325
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Saurav Luthra, MD,MBBS
A RARE CASE OF HYPERAMMONEMIC ENCEPHALOPATHY SECONDARY TO
VALPROATE TOXICITY
First Author: Saurav Luthra, MD,MBBS Vasvi Singh, MD Carlos Palacio, MD
Introduction: Valproic acid (VPA) indirectly increases the amount of gamma-aminobutyric acid (GABA)
available to the central nervous system (CNS). It also alters fatty-acid metabolism, impairs mitochondrial
beta-oxidation, and disrupts urea cycle that leads to hyperammonemia. We present here our experience
of managing a rare case of hyperammonemic encephalopathy from VPA overdose.
Case Description: A 38 year old male with bipolar disorder and presently going through marital
problems was found on the floor of his father’s basement unresponsive, with an empty bottle of VPA
next to him. It was filled 1 week ago with 60 tablets. On admission, vitals were notable for an oral
temperature of 36.1 degree Celsius. He was unconscious, minimally responsive to noxious stimuli and
pupils were pinpoint. Cardiopulmonary, abdominal and skin exam were normal. Labs were notable for
mixed high anion gap metabolic acidosis and respiratory acidosis. Urine toxicology screen was positive
for cocaine, ETOH level was 0.03, and acetaminophen and salicylate levels were negative. VPA level on
admission was 1463 mg/L (normal: 50-100 mg/L) and serum ammonia was 263 mcg/dL (normal: 28-80
mcg/dL).
Chest X-ray and Non-contrast CT head were normal. He was intubated in the intensive care unit (ICU) for
airway protection, and received levocarnitine therapy and emergency hemodialysis the same day as
recommended by the poison control. Post-dialysis, VPA level came down to 250 mg/L and then 125
mg/L on day 2. Ammonia levels also normalized. Patient was extubated on day 3 and discharged to
inpatient psychiatry after 5 days of ICU stay.
[Date]
Discussion: Severe VPA poisoning may present with hypothermia, refractory hypotension, confusion,
lethargy, hallucinations and coma, along with dose dependent respiratory depression that may require
mechanical ventilation. Hyperammonemic encephalopathy is an unusual complication and results from
inhibition of carbamoyl phosphate synthetase-I that begins the urea cycle. Hyperammonemia leads to
increased brain glutamine level that causes astrocyte swelling and cerebral edema. Management is
mainly supportive. Decontamination and elimination may be required. Hemodialysis decreases VPA
levels and should be initiated promptly when levels exceed 850-1000 mg/L. Long-term use of VPA is
associated with serum carnitine depletion, which leads to hyperammonemia. Carnitine also plays a
direct role in metabolism and elimination of VPA. Levocarnitine supplementation is believed to provide
benefit in VPA toxicity, particularly with concomitant hyperammonemia, encephalopathy, or
hepatotoxicity. It is best administered in consultation with a poison control center for dosing
recommendations. More experience is needed before levocarnitine use for valproate toxicity becomes a
standard of care. This case is unique; with remarkably high levels of acute VPA toxicity that responded
very well to our therapy of intensive supportive care, emergent hemodialysis and levocarnitine therapy,
and will add to the knowledge to other physicians facing similar presentation.
326
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Suman Majumdar, MD
Irreversible Paraplegia in a Systemic Lupus Erythematosus(SLE) Patient
Suman Majumdar, Julius Birnbaum, Rithika Menezes, Sakshi Jasra
A 46-year old Caucasian female with SLE presented for evaluation of paraplegia. Two months prior to
the onset of neurological symptoms, she developed active SLE symptoms (low-grade fevers, a
photosensitive rash, polyarthritis, and aphthous ulcerations). Her labs included ANA-antibodies,
elevated anti-double stand DNA antibodies, anti-Ribonucleic Protein and anti-Smith antibodies, with
hypocomplementemia. A complete blood count revealed only leukopenia.
Three weeks prior to neurological symptoms, she noted difficulty initiating her urinary stream, and
described a sensation of incomplete emptying. Four days prior to onset, she experienced an acute
onset of back pain, nausea and vomiting, and was admitted for dehydration. During day four of her
admission, she fell while ambulating and was unable to move her lower extremities. A neurological
examination at that time revealed flaccid paraplegia, arreflexia of her lower extremities, and a sensory
cord level at T10. MRI showed a longitudinally extensive lesion spanning the entire spinal cord.
However, T2 hyperintensity was restricted to the gray matter in the central part of the spinal cord.
Furthermore, the lack of enhancement on T1 post-Gadolinium sequences was suggestive of venous
infarction. Lumbar puncture excluded infection.
Patient was diagnosed with “lupus myelitis”, and treated with pulse 1000 milligrams intravenous
methylprednisolone for five days. Sequential neurological examinations revealed persistent flaccid
paraplegia, and she underwent seven cycles of plasma exchange, followed by Rituximab 1000 milligrams
administered two weeks apart. Unfortunately, she had persistent flaccid paraplegia, was relegated to a
wheelchair, and discharged to a rehabilitation facility.
[Date]
Myelitis is increased 1000-fold in patients with systemic lupus erythematosus (SLE) versus the general
population, and can result in severe neuropathic pain, weakness, and sphincteric deficits. Although
lupus myelitis is traditionally considered a demyelinating mechanism, a subtype of “gray-matter”
myelitis has been shown to represent venous infarction. As illustrated in our patient, SLE patients with
gray-matter myelitis suffer explosive onset of irreversible paraplegia, and have MRI neuroimaging
studies supporting venous infarction. Furthermore, SLE patients with gray matter myelitis
invariably present with difficulty voiding hours to days prior to onset of paraplegia. This is a potentially
treatable prodrome (also seen in our patient), with important mechanistic implications, given that
sphincteric tracts constitute the watershed zone of the spinal cord. Therefore, recognition that SLE
myelopathies may represent venous infarction, not demyelinating disease, suggests that urinary
retention is a potentially treatable prodome to prevent irreversible paraplegia.
327
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Kaushik Mandal, MD
STEMI of a rarest etiology: an unusual case report
First Author: Kaushik Mandal, MD; Apurwa Karki, MD; Riteshkumar Patel,MD; Aditya Mangla, MD.
Department of Medicine, Jamaica Hospital Medical Center, NY.
Introduction: Approximately 90% cases of MI are due to acute thrombus. Other causes involve coronary
occlusion secondary to vasculitis, valvular disease, emboli etc. Congenital pericardial defect is a rare
clinical entity which may present as angina, palpitation and rarely as catastrophic condition posing
diagnostic dilemma.
Case Description: A 43- year-old male presented in the ER with sudden onset of chest pain at rest. The
pain was graded 10/10, typical chest pain with mild discomfort in breathing and was not relieved with
nitroglycerin. Patient had no known significant past medical illness. Patient is non smoker, non alcoholic,
denied drug abuse. Vitals were remarkable for elevated BP:179/114. Physical examination revealed well
developed obese male in severe distress. The initial ECG revealed sinus rhythm, normal rate (84) with ST
elevation in lead I, aVL, II, V4-V6. Labs were significant for elevated Troponin-I: 11.1 (normal :<0.033
ng/ml) with normal creatinine clearance. Diagnosis of acute STEMI was made.
Immediate cardiac catheterization revealed multiple filling defects in left circulation system. There was
two vessel diseases involving LAD and Left circumflex. In the distal LAD there was 99% stenosis. In 1st ,
2nd and 3rd Diagonal there were 95 % stenosis each. In 1st obtuse margin and 2nd Obtuse margin there
was a 95 % and 90% stenosis respectively. LV grams revealed overall normal EF. An immediate
impression was multiple embolic thrombi which occluded these vessels and PCI was attempted on the
culprit lesions. Thrombectomy was performed on distal LAD and 2nd Diagonal lesions with balloon
angioplasty which were unsuccessful with 95% residue. Final conclusion post procedure was
compression of coronary vessels OM1, OM2, LAD and diagonal distal part from external source. To
confirm diagnosis immediate structural evaluation of heart was performed with imaging studies. CT
images showed a cardiac lesion with increased attenuation arising from the apex. MRI further
confirmed constricted apex due to herniation through the existing partial pericardial defect. Urgent left
thoracoscopy was performed, an obvious defect in the pericardium indentified and herniation of the
heart was confirmed. A left mini thoracotomy was performed to release the constriction imposed over
the heart with improvement in circulation.
[Date]
Discussion: In conclusion, an angiographic intervention finding such as in this case with linear
circumferential obstruction should raise a suspicion of cardiac herniation. The differentials of such
would be left ventricular aneurysm, cardiac tumor, pericardial tumor, thoracic tumor etc. Imaging
should be performed in such cases and intervention should be done early before incarcerated hernia
develops to prevent irreversible myocardial damage, cardiogenic shock and death.
328
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Jessica J Patel, MD
Parotid MALToma as the Initial Presentation of Sjogren’s Syndrome
First Author: Jessica J Patel, MD; Shreya Sinha, MD; Arunpreet Kahlon, MBBS; Ivan Marchena, MD; Hom
Neupane, MD
Introduction: Sjogren’s syndrome has a strong association with the transformation of benign epithelial
tissues into malignant lymphomas, such as mucosa-associated lymphoid tissue lymphoma. We present a
case in which malignancy preceded the discovery of an underlying autoimmune pathology.
Case Description: Eight years ago, a 32-year-old man presented to the clinic with a soft, rubbery mass
behind his right pinna, in which pathology showed benign lymphoepithelial lesions. At that time, the
mass and entire right parotid gland were resected. He remained asymptomatic until age 40, when he
developed another palpable mass, now in the left parotid gland. Left partial parotidectomy was carried
out, with removal of 1.6 cm oval-shaped mass and partial deep facial nerve. Histology revealed a low
grade B cell Non Hodgkin’s Lymphoma, MALT lymphoma. Contrast-enhanced CT scan of the chest,
abdomen, pelvis, and PET scan illustrated regional nodes bilaterally in the neck, 1 cm right
submandibular lymph node and 1.2 cm irregularity in the left parotid bed, staging the MALToma as
IIE. Patient was referred for definitive radiation; he declined due to developing xerostomia, which
would worsen with radiotherapy.
Six months later, patient complained of severe, persistent dry eyes and mouth, and weight loss due to
poor appetite. He started developing fatigue and bilateral synovitis of his hands. Repeat imaging for
surveillance was unchanged. Rheumatic serology was negative for rheumatoid factor, however strongly
positive for SSA/Ro, SSB/La autoantibodies. Lacrimal gland dysfunction was evidenced by a positive
Schirmer’s test, confirming Sjogren’s syndrome. Hydroxychloroquine sulfate was started in light of
arthritic symptoms, followed by methotrexate and prednisone when the former proved to be
ineffective. The patient’s symptoms have since improved, and there has been no recurrence or systemic
disease detected secondary to MALToma.
[Date]
Discussion: One of the most serious complications of Sjogren’s syndrome is malignant lymphoma,
however the pathogenesis of autoimmune disorders leading to malignancy remains unclear. It is
thought that B-cell activation and lymphocytic infiltration seen in Sjogren’s causes autoimmunity and
reaction with benign epithelial tissue, leading to immunoglobulin disturbances, which disrupt tumor
suppressor genes and apoptosis causing malignancy. In this case, patient initially had lymphoepithelial
lesions of the right parotid and eight years later MALToma on the left. During the interim, he did not
have symptoms of dry eyes, dry mouth or arthralgia until six months after resection of left parotid
gland. This case has provided an atypical presentation of Sjogren’s in which malignancy appeared
before the full blown disease, thus autoimmune causes should be in the differential diagnosis for
lymphoproliferative malignancy.
329
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Bradley William Petkovich, MD
A RARE CAUSE OF REFRACTORY ASCITES - A REMINDER THAT SEEING IS BELIEVING
First Author: Bradley William Petkovich, MD Second Author: Kerry Schaffer, MD Third Author: John
Grable, MD
Introduction: Ascites, the pathological accumulation of fluid in the peritoneal cavity, is commonly
encountered in medical practice. It is frequently associated with liver disease, congestive heart failure,
inflammatory conditions, or neoplasms. We present a case of non-portal hypertensive, exudative
ascites to review the systematic approach to ascites and to highlight the need for aggressive diagnostic
techniques when preliminary tests and imaging are negative.
Case: Mr. S is a 55 year old gentleman with a past medical history remarkable for atrial fibrillation on
warfarin, hypertension, type 2 diabetes, and multiple stable pulmonary nodules. Mr. S developed
severe refractory ascites in the setting of an IR guided biopsy of a 2 cm posterior left kidney nodule as
part of a work up for microscopic hematuria. The biopsy showed atypical cells mixed with lymphoplastic
inflammation consistent with a reactive process. Days after this procedure, the patient developed new
onset abdominal pain, distention and ascites not seen on the previous two CT scans. Initial work-up for
the ascites revealed a Serum – Ascites Albumin Gradient (SAAG) of <1.1, ascites total protein of 3.1, an
ascitic: serum creatinine ratio of 1.03, no malignant cells on cytology, with normal amylase, lipase, and
triglyceride levels. A liver ultrasound was normal for hepatic flow and liver architecture. After a renal
nephrostogram revealed a small amount of contrast extravasation, a left proximal ureter stent was
placed. However the patient continued to require multiple taps for rapidly accumulating ascites with a
net 30 L of ascites removed over a two week period. These further ascites evaluations continued to
demonstrate negative acid fast bacilli stain and culture, negative bacterial or fungal growth, negative
cytology and tumor markers (CEA, CA-19-9 and AFP), with low triglycerides, and normalization of the
ascitic: serum creatinine ratio to < 1. As our patient continued to decompensate and accumulate ascites
without a diagnosis, Surgical Oncology was consulted to perform a diagnostic laparoscopy. Biopsies
from surgery revealed a high-grade angiosarcoma lining the omentum. The angiosarcoma had not been
visualized on the four previous abdominal/pelvic CT scans. Repeat biopsy of the initial posterior kidney
nodule showed entirely necrotic tissue. With a poor performance status, the patient was not a
candidate for systemic chemotherapy and eventually died of complications from his massive fluid shifts
while under palliation.
[Date]
Discussion: Angiosarcomas are typically considered rare skin/soft tissue cancers of endothelial origin
accounting for 1-2 % of all cancers with even fewer cases involving the gastrointestinal tract. Refractory
ascites is a common condition seen by hospital physicians. This case of refractory non-portal
hypertensive ascites of a rare diagnosis serves as a reminder that when ascites labs continue to lean
towards malignancy, directly visualizing the peritoneum with diagnostic laparoscopy can be invaluable.
330
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Darya Rudym, MD
“All Smoke, no Mirrors”: Pulmonary Langerhans Cell Histiocytosis in Smokers
Darya Rudym MD, Jack C. Naggar MD, Mitchell Charap MD
Introduction: Pulmonary Langerhans Cell Histiocytosis (PLCH) is a rare histiocytic disorder that presents
with nonspecific pulmonary and constitutional symptoms. Given the dearth of specific symptoms and
the rarity of the disease, making the diagnosis remains challenging.
Case Description: A 62 year-old male, 80 pack-year smoker with Gold Stage 4 COPD, presented to his
primary medical doctor for follow up. He has been compliant with his medications. He reported no
change in his usual daily cough productive of white sputum but noted a decrease in his exercise
tolerance from a baseline of half to a quarter of a block, limited by dyspnea. He also described feeling
more fatigued and reported significant night sweats. Chart review revealed four admissions for COPD
exacerbations in the last six months. A 30-pound weight loss was noted over the same time period. His
exam revealed a chronically ill appearing man with diffuse rhonchi bilaterally but no lymphadenopathy.
He was referred for Computed Topography (CT) of his chest out of suspicion for lung cancer. CT chest
was notable for peripheral airway wall thickening with retained secretions as expected, but showed no
evidence to suggest a lung neoplasm. Few low-density foci of unusual configuration with definable walls
and few small scattered ill-defined nodular opacities, most pronounced in upper lobes, were
appreciated. The constellation of these radiographic findings suggested PLCH. The patient was
counseled on smoking cessation, prescribed corticosteroids and referred to a pulmonologist.
[Date]
Discussion: Pulmonary Langerhans Cell Histiocytosis is a disease entity classified under a group of
smoking related interstitial lung diseases. Initial presenting symptoms are often worsening cough and
dyspnea that can be easily mistaken for COPD exacerbation, especially in chronic smokers. Presence of
additional constitutional symptoms, however, should suggest PLCH. It should be recognized that vast
majority of patients with PLCH are long-term smokers. While chest x-ray can be normal or have
micronodular infiltrates, CT is essential for diagnosis. Diagnostic findings include peribronchiolar
nodules, cavitated nodules, and cysts with relative sparing of lung bases. Definitive diagnosis is made
with greater than five percent CD-1a positive cells on bronchoalveolar lavage. Despite its rarity, PLCH
should be considered in the differential diagnosis in an active smoker who presents with chronic
pulmonary symptoms and weight loss. Provider continuity and careful chart review were instrumental in
assuring further investigation and arriving at the correct diagnosis in this case.
331
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Gokul Samudrala, MD
A RARE CASE OF ACUTE MYOCARDIAL INFARCTION SECONDARY TO CORONARY
EMBOLISM IN A PATIENT WITH NON-ISCHEMIC CARDIOMYOPATHY
First Author: Gokul Samudrala, MD, Abigail Quintos MD, Tejan Patel MD, Michael DiSalle MD.
Department of Medicine, Department of interventional cardiology, Rochester Regional Health System,
Rochester, NY.
Introduction: Coronary embolism is a rare cause of acute myocardial infarction (MI). We are reporting a
case of MI due to coronary embolism in a patient with Non-Ischemic Cardiomyopathy (NICM).
Case Description: Patient is a 75 year old female with a medical history of NICM with an ejection fraction
(EF) of 10-15% first diagnosed in 2008. At that time an angiogram revealed normal coronaries and
echocardiogram showed normal heart valves. Patient was admitted in 2014 for decompensation of her
systolic congestive heart failure (CHF). While being treated for CHF, she suddenly developed new onset
throat pain, followed by chest pain radiating to her left arm. Vitals at that time were notable for HR 92,
BP 110/72, RR 18, Temp 98.4F and Spo2 100% on room air. EKG revealed left bundle branch block (LBBB)
and was similar to her baseline EKG except for nonspecific T wave inversions in Lead I and V6 and mild
ST segment elevations of the inferior leads. Troponin-I were 0.11,2,78 and peaked at 152. Emergent
coronary angiogram revealed 100% occlusion of left obtuse marginal branch (OM1). Per cutaneous
transluminal coronary angioplasty followed by embolectomy resulted in complete recanalization of the
OM1. No atherosclerotic plaques were seen in any coronary arteries. Transthoracic Echocardiogram did
not demonstrate any intra cardiac thrombus. Considering the fact that the patient had normal sinus
rhythm, no valvular heart diease nor intracardiac thrombi, it was concluded that this embolus arose
from the left ventricle given the severely depressed EF. Patient was anticoagulated with warfarin before
discharge to home.
[Date]
Discussion: It is a well-established fact that myocardial infarction can occur due to coronary embolism
especially in patients with known history of mechanical valve replacement with inadequate
anticoagulation, bio-prosthetic mitral valve, hypertrophic cardiomyopathy, atrial fibrillation with or
without valvular heart disease and intramural thrombi. Coronary embolism in non-ischemic
cardiomyopathy is extremely rare. An extensive search of literature revealed no case reports of MI
secondary to coronary embolism in patients with NICM, normal valves, normal sinus rhythm and
without intracardiac thrombi. Current guidelines recommend anticoagulation for at least 3 months in
patients with LV dysfunction and intracardiac thrombi. However, there are no current guidelines on
patients with embolic events and no intracardiac thrombi.
332
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Najamus Sehar, MD
Collapsing Focal Segmental Glomerulosclerosis in an HIV negative, Acute Malaria
infected patient
First Author: Najamus Sehar, MD, MPH Emad Gobran, MD Suzanne El-Sayegh, MD
Introduction: Collapsing Focal segmental glomerulosclerosis (FSGS) is most commonly seen in
association with HIV infection. In a few case reports, collapsing FSGS has been described in relation to
other infections like CMV, Parvovirus B1, Pulmonary TB and Leishmaniasis. Rare data is available about
the association between Collapsing FSGS and Malaria.
Case description: A 72 year old African male patient presented to the hospital for generalized body
aches, fatigue, fever and night sweats for three days. He had history of recent travel to Ghana and
returned to the USA ten days prior to symptom onset. Past medical history included gout and
hypertension. Initial physical exam was significant for BP of 186/99 and Temperature of 102o F. Patient
looked in acute distress and was shivering. Laboratory tests showed elevated serum Creatinine (Cr) of
2.09 (baseline was 1.5 in 2012). Hospital course was significant for rapid elevation of Cr to 9.5 and
proteinuria (7.9 gm). Autoimmune workup was negative. Blood smear resulted positive for Plasmodium
Falciparum and patient was treated with Artemether/Lumefantrine. Patients fever and pain improved
but kidney function continued to deteriorate and he became oliguric. On day seven, he was started on
Hemodialysis. He underwent left kidney biopsy which revealed 8 glomeruli, 3 of which were globally
sclerosed and 4 of the remaining glomeruli displayed lesions of collapsing glomerulopathy which ranged
from segmental to global. Biopsy also showed collapse of the glomerular tufts and prominent
hyperplasia of overlying epithelial cells as well as interstitial fibrosis. Findings were consistent with
severe collapsing glomerulopathy.
[Date]
Discussion: Collapsing FSGS carries the worst prognosis among all five types of FSGS. This case illustrates
a biopsy proven Collapsing FSGS likely secondary to Malarial infection with rapid deterioration of kidney
function to the point of requiring renal replacement therapy. Literature review revealed only few case
reports done in Africa that suggested the possible association of Malaria to secondary form of FSGS.
333
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Sumaira Shafi, MD
DIFFUSE LARGE B CELL LYMPHOMA PRESENTING AS ISOLATED SPLENOMEGALY.
Sumaira Shafi MD, Cristian Papazoglou MD, Zhenyang Jiang MD, Munima Shaikh MD, Prasanta Basak
MD, Stephen Jesmajian MD
Hematological disease accounts for approximately 16–66% of all cases presenting with splenomegaly in
USA. Most common diagnoses include lymphoma, CML, CLL, Hemoglobinopathy and Myelofibrosis.
Primary splenic lymphoma is a rare disorder with an incidence of <1 %. Diffuse large B cell lymphoma
(DLBCL), most common subtype of Non Hogkins Lymphoma, usually manifest as lymphadenopathy. We
report a case of DLBCL presenting predominantly with splenomegaly.
A 58 year old male presented with 10 months history of fever, weight loss and upper abdominal
discomfort. In the past, he was treated with INH for presumed latent tuberculosis, doxycycline for
possible tularemia, atovoquone and azithromycin for possible babesiosis with persistent symptoms.
Physical examination was unremarkable except of pallor and palpable spleen. There was no fever or
palpable lymphadenopathy. Laboratory data showed Hb: 8.2g/dL, WBC 8600/µL with normal
differentials, platelets 273,000/µL, microcytosis and anisocytosis. Serum electrolytes were normal. LFTs
showed albumin of 2.9g/dL, AST 72U/L, LDH 1,047 U/L, B2 microglobulin 4.2µg/mL, ESR 50mm/hr, CRP
95.4mg/L. CT chest abdomen and pelvis showed homogenous hepato-splenomegaly with no focal
lesions in the liver or spleen. Blood and urine cultures were negative. Peripheral blood smears and
serology were negative for parasites and Lyme disease. HIV and Miliary tuberculosis were ruled out.
Echocardiogram was normal. Bone marrow biopsy showed normocellular marrow with trilineage
hematopoiesis. After 12 months of illness, a 2 cm firm lymph node was palpable in the right axilla.
Histopathology of the lymph node showed B cell type germinal center and positive
immunohistochemistry markers consistent with DLBCL.
Lymphoid malignancies that can present with isolated splenomegaly include marginal zone lymphomas,
splenic diffuse red pulp B-cell lymphoma or primary splenic nodal lymphomas like DLBCL. Symptoms of
primary splenic lymphoma include fever, weight loss, generalized weakness and left upper quadrant
pain. Significant laboratory findings include cytopenia, elevated ESR, LDH or B2 microglobulin levels.
[Date]
In absence of lymphadenopathy, isolated splemnomegaly can be a diagnostic challenge. In the setting of
positive B symptoms and splenomegaly, primary splenic lymphoma should be considered as a
differential and splenic biopsy may be indicated in such cases.
334
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Yash Shravah, MD
Smoking - What is it good for?
Yash Shravah, MD., Roxana Elena Lazarescu, M.D.
Introduction: Tobacco is an extremely well studied substance with many detrimental side effects,
however its beneficial effects are less well understood. There are many harmful products within tobacco
plant itself, most notably the addictive alkaloid nicotine. However, there are other compounds that are
less well studied such as anatabine. Anatabine is a minor alkaloid found in the same tobacco plant that
has recently started to be studied. There appears to be a lower prevalence of Hashimoto's thyroiditis in
tobacco smokers.
Case Presentation: This is a 58-year-old male with a past medical history of hypertension,
hyperlipidemia, and sudden cardiac arrest 4 months ago, who presented with an inability to chew. Jaw
weakness was associated with generalized weakness, fatigue, muscle tightness, severe tiredness, and
increased sleepiness for the past 4 months. Patient also complained of dyspnea on exertion and
occasional chest pain. He stopped smoking 4 months ago following sudden cardiac death in Russia (as
per patient with extensive work-up and unclear etiology). He also says he has a 10-12 pound weight gain
since smoking cessation. He denies hematuria, dysuria, constipation, unusual hair loss, or fever. He also
denied illicit drug use (no cocaine, heroin, marijuana, amphetamines), and had no alcohol use. Vital
signs were unremarkable as well as was physical exam including thyroid examination. Labwork was
significant for elevated creatinine kinase, low thyroid stimulating hormone, and strongly positive antithyroid peroxidase antibodies.
[Date]
Discussion: Smoking seems to induce changes in thyroid function tests, like a decrease in TSH and
increase in thyroid hormones. In Hashimoto's disease, a lower prevalence of thyroglobulin antibodies,
thyroperoxidase antibiodies and hypothyroidism were found in smokers. Carlé A et all assessed in a
recent study the association between smoking habits (smoking cessation in particular) and development
of autoimmune hypothyroidism. Incidence of hypothyroidism was very common in people who had
recently stopped smoking. Results were consistent in both sexes and irrespective of age. Within two
years after smoking cessation, the percentage of hypothyroid cases attributable to cessation of smoking
was 85%. In conclusion, the risk of having overt autoimmune hypothyroidism diagnosed was more than
6-fold increased the first 2 years after cessation of smoking. However the component that is responsible
for such effects has only recently been suggested to be the minor alkaloid anatabine. There are several
studies that have shown a benefit to the use of anatabine in mice. Currently there are ongoing studies
called the ASAP human thyroid study which is looking at the effect of taking supplemental anatabine in
thyroid disease. While this was a randomized control trial showing beneficial effect of anatabine, it was
performed with a low power
335
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Pramod Theetha Kariyanna, MD
Myocardial Ischemia following Intracavernosal Phenylephrine Injection for
Priapism secondary to Tamsulosin
First Author: Pramod Theetha Kariyanna Tamera Akarah, B.S., Hardik Patel M.D
Introduction: Priapism is a rare side effect of Tamsulosin. Phenylephrine, an alpha-agonist is commonly
used to treat tamsulosin induced Priampism. We here report a case of NSTEMI following intracavernosal
phenylephrine that was injected to treat tamsulosin induced priapism.
Clinical Vignette: A 71-year-old black male presented with painful priapism of 6 hours duration, which
was not relieved by ice-packs application. He had a past medical history of BPH, HTN, and DM for which
he was on Tamsulosin (for 4 years), Enalapril, and Metformin. He stopped taking all his medications 6
weeks before the symptom onset, as he felt “asymptomatic”. However, upon relapse of BPH symptoms
he took double (0.8 mg) the regular dose of Tamsulosin the night before the onset of priapism. Physical
examination revealed tender, rigid penile erection without any signs of trauma. He was given terbutalin
without any relief followed by right corpus cavernosum aspiration with 18 G needle, which revealed
ischemic priapism and helped to provide brief relief. Then he was given intracavernosal phenylephrine
injection, which helped to achieve detumescence. However, within an hour of phenylephrine
administration, he developed palpitations. EKG revealed sinus tachycardia with mild ST segment
depression in leads II and V6. Laboratory findings demonstrated significant elevation of Troponin-I. He
was diagnosed to have NSTEMI. Medical management followed by successful PCI and stent placement in
the obtuse marginal branch of LCX was done.
[Date]
Discussion: Tamsulosin is a selective a1A receptor antagonist that is prostate specific, but is known to
have effect on corporal smooth muscle. Alpha blocker’s (AB’s) directly inhibit sympathetic stimulus for
detumescence. Tamsulosin is the only AB know to improve sexual function, priapism is viewed as one
end of this effect. Priapism in patients on Tamsulosin usually follows a high dose or with concurrent use
of medication that inhibits its metabolism. Phenylephrine, a pure alpha agonist is the drug of choice, as
it has minimal cardiovascular effects. Myocardial infarction following Phenylephrine administration is
likely due to systemic vasoconstriction causing reflex bradycardia and low cardiac output, which in turn
reduces coronary blood flow, especially in elderly patients with pre-existing CAD. Furthermore,
peripheral vasoconstriction increases afterload and hence increases myocardial oxygen demand. This
phenomenon could have led to the precipitation of myocardial infarction in this patient. This case is
remarkable as ischemic priapism is very uncommon side effect of Tamsulosin. In addition, a literature
review revealed no previous reports of myocardial ischemia following intracavernosal Phenylephrine
injection. The case exemplifies unique challenges that are encountered even with the use of common
medications. It is also an eye-opener that necessitates vigilance during the use of drugs that can
precipitate myocardial ischemia, especially in high-risk elderly patients.
336
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Sharmila Tilak, MD
Tell me where you have been so I can tell you what you have
First Author: Sharmila Tilak, MD Second Author: Roxana Lazarescu, MD
Introduction: In today’s society with migration and tourism on a rise, a clinician must carefully consider
demographics and exposures in clinical decision making to facilitate timely diagnosis and institute
appropriate therapeutic measures.
Case Presentation: 44-year-old male, smoker with no past medical history who emigrated from Greece
three months prior, presented to the ED for severe anemia. The patient reported several weeks of
subjective fevers, chills, night sweats, generalized malaise, unintentional weight loss and worsening
epigastric pain. He first noted severe left upper quadrant abdominal pain four months prior while in
Greece, which resolved. Routine blood tests were within normal limits then. He subsequently developed
postprandial epigastric pain controlled with antacids. Patient was febrile and tachycardic on
presentation. Initial blood tests showed significant pancytopenia with bandemia and reticulocytosis,
however no evidence of hemolysis or disseminated intravascular coagulation. Fecal occult blood test
was negative. Patient was started on broad-spectrum antibiotics however failed to defervesce. Extensive
infectious disease workup was unrevealing for any bacterial, fungal or acute viral infections; including
tuberculosis and HIV. Bone marrow biopsy showed no morphological or immunophenotypic evidence of
EBV infection, carcinoma or lymphoma. An atypical lymphoid population was detected on peripheral
blood smear; however T-cell receptor gene rearrangement studies were negative. Serum protein
electrophoresis showed hypergammaglobinemia. Rheumatologic workup was inconclusive and the
patient failed to respond to steroid therapy. Throughout hospitalization, the patient continued to be
febrile and subsequently developed transaminitis with significant splenomegaly. CT of the abdomen and
pelvis showed markedly enlarged spleen. CT-guided liver biopsy showed benign liver parenchyma.
Patient was planned for diagnostic and potentially therapeutic splenectomy since he became blood
transfusion-dependant. Further discussion with an infectious disease specialist in Greece revealed
recent outbreak of Leishmaniasis in local communities. A bone marrow biopsy was repeated, confirming
the diagnosis of Leishmaniasis by protein electrophoresis. Patient completed a course of liposomal
amphotericin B with resolution of fever, splenomegaly and pancytopenia.
[Date]
Discussion: Our patient presented with fever of unknown origin and was subjected to extensive multiorgan system investigations with proposed splenectomy for a condition commonly encountered and
easily treated in his native country. Leishmaniasis has been classified as a Neglected Tropical Disease – a
group of parasitic and bacterial diseases which have been essentially eliminated in developed countries
however cause significant illness in more marginalized, developing communities affecting more than one
billion people worldwide1. The literature however demonstrates a rise in imported leishmaniasis in
developed, non-endemic countries over the past decade, resulting from increased international tourism,
military operations, and immigration from endemic countries.2 Careful consideration of demographics
and exposures in clinical decision making facilitates timely diagnosis and institution of appropriate
therapeutic measures.
337
NEW YORK POSTER FINALIST - CLINICAL VIGNETTE Mazen Zaarour, MD
MAS: A Can’t Miss!
First Author: Mazen Zaarour, MD 1 Chanudi Weerasinghe MD 1, Joseph Mosak MD 2 1Department of
Medicine, Staten Island University Hospital, Staten Island, NY 2Division of Rheumatology, Staten Island
University Hospital, Staten Island, NY
Macrophage activation syndrome (MAS) is a hyper-inflammatory condition characterized by a cytokine
storm. Cytokines act on macrophages causing hemophagocytic conversion and expansion with multiorgan infiltration. Patients typically present with acute febrile illness, diffuse lymphadenopathy,
hepatosplenomegaly, liver dysfunction, neurologic symptoms, low ESR, and extremely high ferritin
levels. MAS is generally considered a form of Hemophagocytic Lymphohistiocytosis (HLH) that occurs in
patients with rheumatologic disorders such as systemic juvenile inflammatory arthritis, rheumatoid
arthritis, and SLE. It is a rare, yet rapidly progressive and life-threatening condition that requires a low
threshold of suspicion, with early diagnosis and prompt initiation of therapy being essential for a greater
likelihood of survival.
We describe a 62yo white female with a prior medical history of long-standing rheumatoid arthritis who
presented with three days of shortness of breath. Additional medical history was significant for
hypertension. On admission, patient was tachycardic and tachypneic with wheezing in her bilateral lung
fields. Non-invasive mechanical ventilation was initiated, upon which her shortness of breath improved.
Chest X-ray demonstrated bilateral pulmonary nodules of unclear etiology. CT chest/abdomen/pelvis
confirmed the presence of pulmonary nodules as well as hilar and inguinal lymphadenopathy. The
patient’s condition deteriorated over the next twenty-four hours requiring mechanical ventilation and
the use of vasopressors. Work-up for sepsis including bronchoscopy was negative for infection. Her
subsequent hospital course was significant for further multi-organ failure, including oliguric acute kidney
injury requiring CVVH, transaminitis of unclear origin, and refractory pancytopenia requiring multiple
transfusions. Given the multi-system involvement, especially the unexplained pancytopenia in a patient
with underlying rheumatoid arthritis, the diagnosis of MAS was strongly considered. This suspicion was
confirmed by the presence of marked hyperferritinemia (36,260 ng/ml) in the setting of low ESR (10
mm/hr). Therefore, treatment with etoposide and dexamethasone was initiated. To further support our
diagnosis, a bone marrow biopsy was performed which demonstrated the presence of histiocytes with
features suggestive of hemophagocytosis. Also in favor of MAS, additional lab work came back showing
elevated serum levels of IL-2 receptor. Unfortunately, despite the early initiation of therapy the patient
expired five days later.
[Date]
As described in our case, MAS presents an extreme diagnostic challenge. Given its similar presentation
to sepsis with a rapid progression to multi organ failure, a high index of suspicion is warranted. The
combination of unexplained cytopenias and extremely high ferritin levels in patients with underlying
rheumatologic disease should make the diagnosis of MAS a strong consideration and treatment should
be initiated immediately, irrespective of confirmatory diagnostic testing.
338
NORTH CAROLINA POSTER FINALIST - CLINICAL VIGNETTE Sean A Marco, MD
Up Against Extremes: The Challenge of Treating Thromboembolism in Obese
Patients After Gastric Bypass
Sean Marco MD, George Sangah MD, Komal Parikh MD
INTRODUCTION: With the growing obesity health epidemic, weight loss surgery is becoming more
common. Both obesity and peri-operative immobilization are independent risk factors for venous
thromboembolism. Despite rising use of novel anticoagulant agents, there remains a paucity of data on
the efficacy and safety of therapeutic anticoagulation in patients of extreme weight with history of
gastric obesity procedures.
CASE DESCRIPTION: A 36 year old Caucasian female with significant past medical history of
hypertension, super obesity and recent gastric obesity procedure with intra-operative infrarenal inferior
vena cava (IVC) filter placement presented to an emergency room with shortness of breath, right groin
pain, and right lower extremity swelling one month after her Roux-en-y gastric bypass. As venous
thromboembolism prophylaxis, she had received 40 milligrams of Enoxaparin subcutaneously twice daily
for 10 days immediately following her gastric bypass. She had no known history of venous or arterial
thromboembolism or known clotting disorder. Exam at first presentation was significant for tachycardia
and hypoxia. Lower extremity doppler ultrasound revealed a large deep venous thrombosis extending
from the right common femoral vein to the right popliteal vein. Computed Tomography Angiography
(CTA) of her chest showed bilateral pulmonary emboli. The IVC filter was visualized radiographically in
the infrarenal IVC. Echocardiogram showed no evidence of right heart strain. She was started on
Rivaroxaban and discharged home on supplemental oxygen. Four days after discharge, she re-presented
to our hospital for worsening shortness of breath and persistent right groin pain. At that time, her body
mass index was 62 and she was hemodynamically stable, without increased oxygen requirement.
Electrocardiogram showed sinus rhythm. Chemical profile and complete blood count profile were
unremarkable. Repeat CTA was not done, out of concern for unnecessary radiation exposure. A Heparin
infusion was initiated and extensive literature review was undertaken to evaluate the appropriateness
of novel anticoagulants for treating obese patients and for treating obese patients with gastric obesity
procedures. The decision was made to stop Rivaroxaban and initiate warfarin therapy with extensive
patient education and close monitoring. Our patient was discharged 4 days after warfarin initiation with
therapeutic international normalized ratio (INR). At 8 week follow up, she was tolerating warfarin and
her INR was stable.
[Date]
DISCUSSION: Our case highlights a rising challenge in medicine; the need for physicians to extrapolate
previously published data to extremes of weight, all in the setting of known alterations in absorption
after gastric bypass. Ultimately, more studies are needed to fully determine the safety, effectiveness
and pharmacokinetics of novel anticoagulants for therapeutic anticoagulation in this special patient
population.
339
NORTH CAROLINA POSTER FINALIST - CLINICAL VIGNETTE Samaya J Qureshi, MD
A Triad of Phenazopyridine Toxicity
First Author: Samaya Qureshi, MD Second Author: Rakesh Alva, MD
Introduction: Phenazopyridine (Pyridium) is a urinary analgesic with side effects including urine and skin
discoloration to more serious reactions including anemia and renal failure. We describe a case of
methemoglobinemia induced hypoxic respiratory failure, hemolytic anemia, and acute renal failure
secondary to Phenazopyridine toxicity. This case is significant due to the occurrence of multiple
coinciding adverse reactions of an over the counter medication. It stresses the importance medication
list review and clinician awareness of common side effects and toxicity of such medications.
Case: A 56-year-old female with anemia, hypothyroidism, bilateral pulmonary emboli on Rivaroxaban,
and interstitial cystitis on chronic Phenazopyridine was admitted for acute respiratory failure. Initial labs
were significant for acute renal failure and acute on chronic anemia. Further investigation revealed
significantly elevated percentage of methemoglobin and evidence of hemolysis with schistocytes on
peripheral blood smear, elevated lactate dehydrogenase, and low haptoglobin. Hospital course involved
packed red blood cell transfusions for worsening anemia and conservative management of renal
failure. With cessation of Phenazopyridine, methemoglobinemia and hypoxia resolved. Anemia and
renal failure also improved and methylene blue was not given.
[Date]
Conclusion: Phenazopyridine is an over the counter medication indicated for the relief of symptoms
such as pain, frequency, and burning associated with irritation of the lower urinary tract
mucosa. Phenazopyridine toxicity is well described in the literature. This case illustrates multiple
simultaneous adverse reactions including hypoxia due to methemoglobinemia, hemolytic anemia, and
renal failure in the setting of chronic Phenazopyridine use. Providers need to remain vigilant in regards
to these serious reactions and educate their patients as well. Prompt recognition of toxicity and
initiation of treatment can lead to improved outcomes and avoid needless testing. Regular review of
medication lists and timely cessation of such agents can prevent similar toxicity events in the future.
340
OHIO POSTER FINALIST - CLINICAL VIGNETTE Julia L Agne, MD
Empiric Treatment of Cytokine Release Syndrome during Septic Shock
First Author: Julia L Agne, MD Robert A Baiocchi, MD, PhD Maria R Lucarelli, MD
Cytokine release syndrome (CRS) is a potentially life threatening complication following adoptive T cell
therapies for the treatment of cancer. Symptoms of CRS often mimic those of severe sepsis, which may
delay anti-inflammatory treatment if not clinically suspected.
A 71 year old woman with history of treatment-refractory diffuse large B cell lymphoma presented to a
local emergency department upon returning from a medical facility in Mexico where she received
autologous immune enhancement cell therapy as adjunctive cancer treatment. The therapy consisted of
a combined infusion of activated T cells stimulated by systemic perfusion hyperthermia and autologous
dendritic cells. Upon completion of the infusion, the patient reported fever, arthralgias, myalgias,
abdominal pain, and back pain, which continued to persist after the patient returned to the United
States 24 hours after the infusion. In the emergency department, the patient was febrile, hypotensive,
and tachycardic. Further laboratory testing revealed leukocytosis (WBC 24,000), hyperkalemia
(potassium 6.0 mmol/L), hyperuricemia (uric acid 10.4 mg/dL), and acute kidney injury (serum creatinine
5.0 mg/dL). Two peripheral blood cultures revealed gram positive cocci in clusters, and transthoracic
echocardiogram revealed a 1 cm aortic valve vegetation consistent with infectious endocarditis. The
patient was fluid resuscitated, required norepinephrine for blood pressure support, and was empirically
treated with IV vancomycin and doripenem for septic shock. Upon transfer to our tertiary care center,
the patient became apneic, requiring intubation and mechanical ventilation.
In light of the patient’s recent adoptive cellular therapy, there was high clinical suspicion for CRS. Serum
C-reactive protein (CRP) level was disproportionately elevated compared to the erythrocyte
sedimentation rate (143 mg/L and 29 mm/h, respectively), an indirect indicator of high serum
concentrations of the interleukin 6 (IL-6) cytokine. Subsequently, serum IL-6 was elevated at 222 pg/mL.
Due to high concern for Grade 4 CRS, associated with a near 100% mortality if untreated, the patient
was empirically treated with high dose dexamethasone (two doses of 40 mg). She was successfully
weaned from norepinephrine within 24 hours and extubated 72 hours after admission.
[Date]
Cytokine release syndrome is a clinical diagnosis associated with elevated levels of multiple cytokines,
including IL-5, IL-13, IL-10, IL-6, and interferon gamma. This case illustrates the difficulty of distinguishing
CRS from septic shock and the importance of initiating anti-inflammatory treatment. Empiric treatment
of CRS was warranted due to the patient’s recent history of autologous T cell infusion. Dexamethasone
is considered second-line therapy after tocilizumab, an IL-6 receptor antibody that was contraindicated
due to the patient’s gram positive infectious endocarditis. Treatment of Grade 4 CRS should not be
delayed due to high incidence of mortality with concomitant septic shock.
341
OHIO POSTER FINALIST - CLINICAL VIGNETTE Amit Arbune, MBBS
Pyogenic Liver abscess: An Unusual Post-ERCP Complication
First Author: Amit Arbune, MBBS Patrick Brine, MD Thomas Marnejon, DO
Pyogenic liver abscess (PLA) is one of the most common visceral abscesses found in patient’s with
underlying hepatobiliary or pancreatic disease. Recently, the incidence of PLA has decreased. Common
etiologies include malignant biliary tract, portal seeding from appendicitis and diverticulitis. We present
an unusual case multiple liver abscesses with streptococcus intermedius as a complication of ERCP.
A 76 year old Caucasian male was brought to the ER due to a fall and altered mental status. The patient's
mentation improved with volume resuscitation, subsequently reported having abdominal pain for ~5
months duration. The pain was described as dull, non-radiating, epigastric and progressively worsening
over the past few months without any aggravating or relieving factors. Patient reported lethargy, fever,
chills, and decreased appetite over the preceding 3 weeks. Denied any nausea, vomiting, diarrhea,
melena, hematochizia, chest pain, or dyspnea. The patient's past medical history included hypertension,
gout, cholelithiasis and colonic polyps. His past surgical history included laparoscopic cholecystectomy
and right knee arthroplasty. He underwent ERCP 5 months prior to admission and colonoscopy 3 years
ago. The patient denied any drug allergies, was a former smoker, denied alcohol and illicit drug use.
The patient’s initial vitals included a temperature of 101.7 degree F, HR 190 bmp, RR 20 per minute and
BP 93/56 mm Hg. Initial laboratory studies showed normal basic metabolic profile, leukocytosis, slightly
elevated transaminases, normal bilirubin, albumin, and total protein. A non-contrast CT abdomen-pelvis
showed fluid in the gall bladder fossa, inflammatory changes around the pancreas, pneumobilia,
multiple hepatic hypodensities, and some fat stranding surrounding the distal aspect of descending
colon.
The patient was treated with volume resuscitation, broad spectrum antibiotics, and subsequently
underwent a repeat CT abdomen with oral contrast which was suspicious for gastric perforation leading
to an exploratory laparotomy. During the procedure, the patient was found to have ascites and multiple
hepatic abscesses which were drained. No gastric perforation was noted. An upper endoscopy was
normal. Blood cultures and culture from the abscesses grew streptococcus intermedius.
In conclusion, this case highlights the importance of having a high index of suspicion for PLA in patient's
post-ERCP, who presents with fever, and abdominal pain, for early initiation of appropriate treatment to
reduce mortality and morbidity.
[Date]
The complication rate of ERCP is 5-15%. The most common being pancreatitis, hemorrhage, perforation
and cholangitis. In a prospective study by of 1,177 ERCP patient’s Christensen et al. from 2004 post-ERCP
infections accounted for only 5% of all complications. Post-ERCP complications were predominantly
cholangitis, however only 1 patient out of 59 was reported to have multiple liver abscesses. We could
only find 2 similar cases in literature. These 2 reported cases described post-ERCP PLA in patients with
intact GB versus our patient.
342
OHIO POSTER FINALIST - CLINICAL VIGNETTE Matthew R Brown, DO
E. coli septic arthritis of the shoulder from an unlikely source: a case report
First Author: Matthew R Brown, DO Second Auther: Adam Fershko, MD Third Author: Sacha
Baldeosingh, MD
A 79-year-old male was admitted to the hospital for altered mental status and right shoulder pain. He
complained of shoulder pain since a fall while climbing stairs 3 days prior to arrival. On physical
examination, the shoulder was swollen, erythematous, warm and had severely limited range of motion.
He was afebrile. Labs revealed a normal WBC. Plain films of the shoulder displayed chronic degenerative
changes. MRI of the shoulder was performed and identified full thickness tearing of several rotator cuff
muscles and the posterior superior labrum. On Day 2 of hospitalization, the patient spiked a fever of
103° F. Blood cultures were drawn and grew E. coli. Orthopedic surgery was consulted and performed a
shoulder aspiration. The fluid was cloudy with the following cell count; WBC 3400 with 93%
granulocytes. Joint fluid culture was positive for E. coli. On Day 4, a CT abdomen was obtained due to his
prior history of rectal cancer status post partial colectomy with subsequent reversal of ileostomy, which
revealed circumferential wall thickening of the rectosigmoid junction. GI was consulted and performed a
colonoscopy revealing an ulcerating rectal mass, which was biopsied and consistent with
adenocarcinoma of the rectum.
[Date]
Septic arthritis is most commonly due to gram-positive species as a result of hematogenous spread.
Most of the time, the affected joint is confined to the lower extremities. The incidence of gram-negative
septic arthritis is 10-15% of documented cases. Shoulder joint involvement constitutes <3% of total
septic arthritis cases and colonic sources (2 case reports of knee involvement, one with S. bovis and one
with C. septicum) are incredibly rare. This case demonstrates a hematogenous seeding of E. coli of the
shoulder from an ulcerated colon mass. The location of infection, source and speciation of this case
highlights a very unusual presentation of a relatively common condition. Further investigation should
always be pursued when unlikely presentations occur in the context of appropriate risk factors and
medical history.
343
OHIO POSTER FINALIST - CLINICAL VIGNETTE Garren J DeCaro, MD
Catastrophic Coagulopathy with Thrombocytopenia after Enoxaparin - It’s Not
Always Heparin Induced Thrombocytopenia
First Author: Garren J DeCaro, MD Second Author: Rex Wilford DO, FACP
Coagulopathy in cancer is relatively common. The standard treatment of venous thromboembolism in
patients with cancer is low molecular weight heparin. However, heparin induced thrombocytopenia
(HIT) is a known side effect of low molecular weight heparins and it should always be considered in any
patient on a heparin product who develops new onset thrombocytopenia and thrombosis. The diagnosis
should be confirmed using HIT antibody testing.
We present a patient with clinically suspected HIT who suffered catastrophic hypercoagulable state due
to underlying malignancy. A fifty one year old female recently diagnosed with metastatic lung
adenocarcinoma and deep venous thrombosis (DVT) of the lower extremity presented with nausea,
vomiting, bilateral flank pain and worsening cognition. Therapy for the malignancy had not been started
yet, she had been started on enoxaparin 6 days prior to presentation in order to treat the DVT. The
patient’s platelet count had dropped from 313 thou/cmm at the time enoxaparin was started to 87
thou/cmm on the day of admission for the DVT. Her physical exam was without focal neurological
deficits, but positive for bilateral flank pain to percussion and general confusion. The abdominal CT
showed multiple bilateral renal infarctions, splenic infarction and right hepatic artery embolus. MRI of
the brain revealed innumerable areas of acute infarction throughout both cerebral and cerebellar
hemispheres. HIT was tentatively diagnosed. Enoxaparin was discontinued and argatroban drip was
started immediately with a rapid therapeutic PTT level reached. Review of peripheral smear by a
hematologist revealed thrombocytopenia and no evidence of microangiopathic hemolysis. On day 3 of
hospitalization the patient developed right sided hemiplegia and aphasia. CTA of the head and neck
revealed no hemorrhage, multiple ischemic changes, and a filling defect in the superior vena cava
thought to represent thrombus. Echocardiography suggested a right atrial mass concerning for
thrombus. The patient developed seizures and respiratory failure and the family opted for comfort care.
The patient died on day 7 of hospitalization. Pending workup revealed both anti-platelet factor 4
antibody and serotonin release assay to be negative, but a positive lupus anticoagulant test (LAHexPhospholipid Neut).
[Date]
This case illustrates ongoing, catastrophic, diffuse coagulopathy in a patient being treated presumptively
for HIT. It is critical to determine the underlying pathological process in patients with thrombosis to best
guide treatment. Lupus anticoagulant has been found more frequently in malignancy and is associated
with increased thrombotic risk. Catastrophic hypercoagulable state of malignancy or antiphospholipid
syndrome should be considered in patients with suspected HIT who continue to have thrombosis
despite recommended therapy.
344
OHIO POSTER FINALIST - CLINICAL VIGNETTE Mohamed Elrifai, MD
A peculiar culprit for acute pancreatitis.
First Author: Mohamed Elrifai, Anna Maria Affan, Suresh Balasubramanian, Keyvan Ravakhah.
Introduction: Lipomas are uncommon pancreatic tumors. They are often found incidentally, and their
association with pancreatitis has not been widely reported. We report a case of acute pancreatitis
caused by a large lipoma of the pancreatic body, diagnosed by computed tomography (CT) and
confirmed histologically.
Case description: A 55-year-old-man with no significant past medical history presented with a 2-week
history of 7/10 constant, dull and deep epigastric pain radiating to the back. It was only alleviated when
he lay flat and still. He denied fever, nausea, vomiting or other constitutional symptoms. He denied any
similar previous episodes. He never smoked or consumed alcohol. He had no past surgeries and denied
abdominal trauma. There was no exposure to toxins or new drugs nor did he have recent infection.
Physical examination revealed a well-nourished male in obvious painful distress. He was tachycardic and
demonstrated epigastric tenderness with voluntary guarding. The bowel sounds were sluggish. The only
significant laboratory finding was an elevated lipase of 7645U/L. Triglycerides were normal. CT abdomen
showed edema of the distal pancreatic body and tail, with surrounding inflammatory stranding
compatible with acute pancreatitis. There was a 1.9cm lesion in the pancreatic body which was noted to
be compressing the main pancreatic duct. Radiological features were consistent with internal fat and
soft tissue attenuation. MRI of the abdomen concluded that the mass was 2.3cm in size with significant
lipid content and well demarcated suggesting a tumor of mesenchymal origin possibly a lipoma or
liposarcoma but given the well demarcated borders lipoma was more likely. The patient underwent
endoscopic ultrasound with biopsy which confirmed the histology as lipoma. He had resection of the
mass to avoid any further episodes of pancreatitis.
[Date]
Discussion: Pancreatic lipomas are rare tumors of mesenchymal origin and until now, the
etiopathogenesis is unclear. Generally, they have an asymptomatic clinical course and are diagnosed
incidentally. However symptoms can arise as the tumor grows causing mass effect which can result in
abdominal pain, jaundice, portal hypertension or, as in our case, acute pancreatitis. Although rare,
pancreatic lipomas are well demonstrated on CT scan. The characteristic imaging features include a
solid, non-enhancing homogenous mass with a clear margin and without any continuity or invasion of
the peripancreatic tissue or organs. The tissue density ranges from –30 to –120 HU (Hounsfield units)
keeping in with the consistency of fatty tissue. Taking into account the benign nature and lack of clinical
manifestation, most cases can escape surgical management. However, in light of compression of the
pancreatic duct, our patient underwent surgical resection to prevent further episodes of acute
pancreatitis.
345
OHIO POSTER FINALIST - CLINICAL VIGNETTE Mohamed Elrifai, MD
A rare cause of infective endocarditis; Pasteurella multocida infection of the
tricuspid valve.
First Author: Mohamed Elrifai, MD Other Authors: Magadia, A, Affan A, Subramanian S, Ravakhah K.
Introduction: Pasteurella multocida is a gram-negative coccobacillus found primarily in the natural oral
flora of animals. It is known to cause localized infections in humans however life threatening infections
are uncommon. We present a rare case of tricuspid valve endocarditis caused by Pasteurella multocida.
Case report: An 86 year old woman with history of mitral valve replacement was admitted for one day
duration of left upper thigh swelling, fever and chills. The patient owned a cat but denied a recent bite
or scratch.
On admission, temperature was 38.2 °C, pulse rate 113 beats/min, respiratory rate 22/min and blood
pressure 164/101. Physical examination revealed a 4x2 cm red patch overlying the left upper thigh with
localized swelling and tenderness. Inguinal lymph nodes were not palpable. Cardiovascular examination
was significant for a grade II/VI non-radiating, systolic murmur located at the left parasternal border.
Her white cell count was 17,200 with 90% neutrophils. Chest roentgenogram and electrocardiogram
were normal. Blood cultures were drawn, preliminary results returned as gram negative coccobacilli
which later confirmed colonies of P. multocida. The bacteria was reported to be susceptible to ampicillin
(MIC 0.25 µg/ml) and ceftriaxone (MIC < 0.25 µg/ml). Due to the patient’s septic presentation combined
with a history of prosthetic valve in situ, transesophageal echocardiogram was done and revealed a
tricuspid valve vegetation.
The patient was initially treated with Ampicillin/Sulbactam 3g IV every 6 hours and discharged on
Ceftriaxone 2g daily to complete a six week course of treatment. Repeat blood cultures prior to
discharge were negative. She remained in good health over the subsequent three months and did not
require surgical intervention.
Clinicians should have a high index of suspicion particularly in high risk patients, as failure to recognize
this condition may lead to devastating outcomes.
[Date]
Discussion: Human infection due to P. multocida has not been only described following animal bites or
scratches but with licking too, mainly from dogs and cats. Bacteremia associated with P. multocida most
commonly accompanies localized soft tissue infection. Complications such as endocarditis are rare and
typically present in immunocompromised patients. To date, only fifteen cases of infective endocarditis
have been reported in literature and generally involve the aortic valves. To our knowledge, this is the
second case of tricuspid valve endocarditis described. Our patient had native tricuspid valve infective
endocarditis based on the modified Duke criteria. However, none of the risk factors traditionally
associated with right-sided endocarditis were present. Infective endocarditis due to P. multocida can be
treated medically based on the susceptibility studies and may not require surgical intervention, however
left-sided infective endocarditis is associated with 30% mortality rate.
346
OHIO POSTER FINALIST - CLINICAL VIGNETTE Madiha Fida, MBBS
Rapidly progressive dyspnea with unexpected autopsy finding
First Author: Madiha Fida,MD Ragheb Assaly, MD Ali Abdulmonam, MD
INTRODUCTION: It can be challenging to find the exact etiology of pulmonary arterial hypertension on
the basis of clinical grounds alone. Here we present a unique case of severe PAH with unexpected
findings on autopsy.
CASE PRESENTATION: A 73 year old man with history of ILD, pulmonary hypertension, asbestosis with
plaques and known heavy exposure to asbestos was admitted with progressive worsening of shortness
of breath (NYHA class IV). Past medical history was significant for coronary artery disease, hypertension,
sleep apnea and atrial fibrillation. Physical exam revealed a systolic murmur accentuated by inspiration,
bibasilar end inspiratory crackles and lower extremity edema. His chest x-ray showed bilateral interstitial
infiltrates with pleural plaques in the left upper lobe. Pulmonary function tests were consistent with
restrictive pattern. Right heart catheterization showed severe pulmonary arterial hypertension with
right ventricular systolic pressure of 113mmHg. V/Q scan was negative for pulmonary embolism. His
DLCO declined from 56% in 2010 to 36% in 2013. On a recent 6 minute walk test, the patient was only
able to walk 22% of his predicted distance. On the second day of admission, he became hypotensive
and subsequently had a cardiopulmonary arrest. Limited autopsy of the heart and lungs ruled out
pulmonary embolism, acute myocardial infarction or significant asbestosis, however, it showed
profound pulmonary capillary hemangiomatosis.
DISCUSSION: Pulmonary capillary hemangiomatosis is frequently misdiagnosed as primary pulmonary
hypertension and pulmonary veno-oclusive disease and the correct diagnosis is not made until autopsy.
Less than 100 cases of pulmonary capillary hemangiomatosis have been reported. In our case, the
interstitial lung disease was secondary to the proliferating microvessels that are prone to recurrent
bleeding leading to hemosiderosis and fibrosis.
[Date]
CONCLUSION: Our case highlights the fact that etiologies other than ILD or OSA should be considered
when pulmonary arterial hypertension is out of proportion to the mild restrictive pathophysiology. The
precise diagnosis of PCH is very important because the treatment with pulmonary vasodilators such as
prostacyclin can cause fatal pulmonary edema.
347
OHIO POSTER FINALIST - CLINICAL VIGNETTE Raktim Kumar Ghosh, MD,MBBS
Papulonodular skin lesions with monocytosis: What is your diagnosis?
Raktim Kumar Ghosh, MD,MBBS Mey Somasundaram MD, Poornanand Palaparty MD, Keyvan Ravakhah
MD
Introduction: Monocytes normally comprise less than 10 percent of total circulating white cells, with the
absolute monocyte count being <800/microL. Persistent monocytosis is associated with certain
hematological malignancies including Chronic myelomonocytic leukaemia (CMML), chronic myeloid
leukemia (CML), acute myeloid leukemia (AML) and hodgkins lymphoma. CMML is a uncommon clonal
haematopoietic stem cell disorder with overlap features of myelodysplastic and myeloproliferative
features. Erythematous papules and nodules on skin are often the only clinical manifestation of this
uncommon malignancy. Skin involvement is regarded as late stage of the disease.
Case: A 84 years old lady, with PMHx of chronic atrial fibrillation and diastolic heart failure presented in
the office for routine 3 months follow up. CBCD showed leukocytosis of 11.8 with 40% monocytes and
normal hemoglobin and platelet. Careful physical examination revealed new onset non ulcerated,
purplish papulonodular lesion on the right leg. Rest of the physical exmination was essentially benign,
including absence of hepatosplenomegaly and lymphadenopathies. Review of 3 months back blood
work showed WBC count of 10.6 and 30% monocytes. Patient was sent for skin biopsy which showed
intradermal infiltrate consisting of large immature appearing myeloid cells with small prominent
nucleoli, sparse basophilic cytoplasm and frequent mitosis, suggestive of leukemia cutis. The infiltrate
was positive for lysozyme, CD 45 and CD 68 but negative for myeloperoxidase. The
immunohistochemical phenotype was most consistent with monocytic origin. Flow cytometry showed
increased monocytosis of 31% but no increase in myeloid blasts. FISH analysis was negative for
BCR/ABL1 translocation. Patient refused bone marrow biopsy. She was diagnosed with CMML after
ruling out CML, AML and MDS. Considering her age and comorbid conditions, allogeneic stem transplant
was not an option. The patient was started on hydroxyurea. At the time of writing this report, significant
reduction in monocyte percentage (19%) and improvement in skin lesions were noted following 2
months of treatment.
[Date]
Discussion: CMML should be suspected when persistent ( >3 months), unexplained peripheral
monocytosis is present in an older adult. Some of the benign causes of monocytosis including
pregnancy, asplenic state, sarcoidosis, major depression, and treatment with corticosteroids need to be
ruled out first. Diagnostic criteria for CMML include peripheral blood monocytosis > 3 months; absolute
monocyte count >1000/microL, greater than 10 percent of the entire white blood cell differential,
absent BCR-ABL1 fusion gene, <20 percent myeloblasts, monoblasts, promonocytes in peripheral blood
and bone marrow. Leukemia cutis is defined as cutaneous infiltration by neoplastic leukocytes resulting
in papulo nodular skin lesions. Skin involvement in CMML patients suggest disease progression.
Allogeneic hematopoietic cell transplantation (allo-HCT) is the only potentially curative therapy for
patients with CMML. Cytoreductive therapy with hydroxyurea is an accepted alternative for patients
who are not candidate for bone marrow transplant.
348
OHIO POSTER FINALIST - CLINICAL VIGNETTE Nilamba A Jhala, MD
Anti-synthetase syndrome associated with cryptogenic organizing pneumonia: Case
report and review of literature.
First Author: Nilamba A Jhala, MD Second Author: Kusuma Kurmayagari MD, Keyvan Ravakhah MD
Introduction: Anti-synthetase syndrome (ASS) is a heterogeneous autoimmune connective tissue
disorder presenting as inflammatory myopathy associated with particular myositis-specific
autoantibodies which are specifically directed against the aminoacyl-tRNA synthetase enzymes. The
organs involved are numerous and diverse, and can vary from patient to patient. We present a case of
ASS associated interstitial lung disease(ILD) and discuss the clinical implications.
Case Description: A relatively healthy 45-year-old African-American man presented with six weekhistory of dyspnea, non-productive cough, low grade fever and fatigue associated with pain & swelling
of extremities for past three weeks. In the meantime, he was evaluated once in clinic and twice in ED
and was treated as a case of community acquired pneumonia(CAP) without any clinical improvement.
Eventually he was admitted for further management. He was afebrile, hypoxic(POx 91% RA) with sinus
tachycardia of 117/min and BP 156/88mmHg . Physical examination revealed dry crackles throughout
bilateral lungs, proximal muscular weakness, mechanic hands and synovitis of MCP, PIP and DIP joints
with trace pitting edema. There was no skin rash, mouth ulcers or palpable mass. The remainder of
physical examination and review of system was unremarkable. Laboratory evaluation was remarkable
for WBC of 12.5, CK > 26,000 K, ESR 72, myoglobinuria, positive RF and anti- Jo antibodies.
Discussion: Anti-synthetase syndrome(ASS) is a systemic autoimmune syndrome characterized by the
presence of anti-aminoacyl t RNA antibodies accompanied by a constellation of clinical findings including
polymyosistis-dermatomyositis (PM-DM), ILD, “mechanic hands” and Raynaud’s phenomenon etc. This
is relatively uncommon clinical entity and is considered as a subset of idiopathic inflammatory
myopathies. Among the anti-synthetase antibodies more frequently associated with lung involvement is
the anti-Jo-1. It is noteworthy that, when present, the lung disease is the main determinant of survival in
patients with ASS. Our patient predominantly complained of respiratory illness, HRCT demonstrated
consolidations consistent with acute ASS associated COP/ILD. This case uniquely demonstrates how the
diagnosis of ASS may not be clinically obvious on initial presentation, but may appear upon further
investigation. We need to consider broad differential diagnosis for suspected infectious pneumonia
cases that are not responding to standard antibiotic regimens. Early diagnosis and treatment can
prevent disease progression and improve patient outcome.
[Date]
Chest radiograph revealed diffuse interstitial thickening in both lungs, predominantly involving the lower
lobes with associated small to moderate bilateral pleural effusions. HRCT revealed multifocal nodular
ground glass opacities and confluent areas of consolidation with mild septal thickening and small to
moderate bilateral effusions suggestive of acute ILD in a pattern observed as cryptogenic organizing
pneumonia (COP). A diagnosis of ASS with COP was made and the patient was started on high dose
corticosteroids. Muscle biopsy was suggestive of polymyositis. Patient did not improve with steroids,
cyclophosphamide was added with significant clinical improvement and was discharged to SNF for
rehabilitation.
349
OHIO POSTER FINALIST - CLINICAL VIGNETTE Sehrish Kamal, MD
Guillain Barre Syndrome and Autoimmune Hepatitis...is there a relationship?
First Author: Sehrish Kamal, MD Muhammad Ali Khan, MD Thomas Sodeman, MD
Introduction: Guillain Barre syndrome (GBS) is a rare clinical syndrome with an estimated incidence of
0.6-4/100,000 persons/year worldwide. GBS commonly occurs in association with infectious agents
likeCampylobacter jejuni, Cytomegalovirus, viral hepatitis, Ebstein-Barr virus, mycoplasma, etc. GBS
can also be associated with mild elevation of alanine transaminase without any known cause. We
hereby report an extremely unusual occurrence of autoimmune hepatitis in a patient with Guillain Barre
syndrome.
Case Presentation: A 24-year-old white male came to the emergency room with complaints of
worsening weakness, numbness, and tingling of distal upper and lower extremities progressing more
proximally. He denied any other symptoms. There was no significant past medical, surgical, social (no
alcohol or smoking), or family history. On examination, he had 1/5 power in bilateral upper extremities
and 2/5 strength in bilateral lower extremities. Upper and lower extremity deep tendon reflexes were
diminished bilaterally. CT and MRI brain did not reveal any acute abnormality. Baseline laboratory
studies including CBC, BMP, INR, and UA were within normal limits. LFTS showed total bilirubin 1.1
mg/dL, direct dilirubin 0.2 mg/dL, ALT 928 U/L, AST 549 U/L, and alkaline phosphatase 205 U/L. Lumbar
puncture revealed elevated protein levels with normal white cell count. EMG nerve conduction study
was consistent with acute inflammatory demyelinating polyneuropathy (AIDP). Ultrasound of liver and
gallbladder were both normal. Viral hepatitis panel including hepatitis A, hepatitis B, hepatitis C, and
hepatitis E were all negative. ANA titers were found to be 1:40, anti-smooth muscle antibody titer 1:80,
liver kidney microsomal antibody titer <1:20; antimitichondrial antibody was not detected.
Ceruloplasmin levels and iron studies were within normal limits. Liver biopsy revealed
lymphoplasmacytic infiltrates in portal tracts with interface hepatitis, hence, the diagnosis of
autoimmune hepatitis was made. During the hospitalization, the patient received IVIG courses for
Guillain Barre syndrome, and for autoimmune hepatitis, he was started on prednisone 60 mg per day,
which resulted in improvement of his liver enzymes. Prednisone was tapered over a course of months,
and azathioprine was added. His liver enzymes normalized over a period of 4 months and he was
maintained on azathioprine.
[Date]
Conclusion:Association of GBS with infectious hepatitis has been widely described in literature. To the
best of our knowledge, this is the first reported case highlighting the unique occurrence of GBS with
autoimmune hepatitis. Hence, autoimmune hepatitis can be considered as 1 of the possibilities in GBS
patients with elevated liver enzymes.
350
OHIO POSTER FINALIST - CLINICAL VIGNETTE Aahd Kubbara, MD
Bilateral Pulmonary Emboli as an Indirect Complication of Gastric Bypass Surgery
First Author: Aahd Kubbara, MD. Danae Hamouda, MD. Shipeng Yu, MD. Youngsook Yoon, MD.
Introduction: Micronutrient deficiencies are a well-known complication of gastric bypass surgery, with
two such micronutrients being vitamin B12 and folic acid. As deficiencies in those vitamins are
associated with increased serum levels of homocysteine, we are reporting a case of a patient who
suffered multiple venous thromboses, with pulmonary emboli, in the setting of vitamin B12 and folate
deficiencies secondary to gastric bypass surgery.
Case Presentation: A 54 year old lady with a past medical history significant for morbid obesity managed
with gastric bypass surgery presented to the ED with nausea and anorexia of 10 days duration.
Associated symptoms included ten-pound weight loss in the prior ten days, exertional dyspnea,
projectile vomiting, and diarrhea. Initial workup in the ED was undertaken. An EKG obtained upon
presentation did not show any acute changes and three sets of cardiac enzymes were within normal
limits, thereby ruling out myocardial ischemia. Further workup included radiographic studies such as a
CT with contrast of the abdomen, which revealed superior mesenteric vein thrombosis in addition to
portal vein thrombosis. CT angiography of the chest was also obtained, which revealed multiple bilateral
pulmonary emboli. Doppler ultrasound of upper and lower extremities did not demonstrate any
evidence of thrombus.
In light of the radiologically proven emboli found, heparin infusion was initiated with an Unfractionated
Heparin “UFH” target of 0.7 U/ml. On the third day of admission, warfarin treatment was begun with
heparin bridge therapy, to complete a course of 3-6 months of anticoagulation therapy.
Further workup during the patient’s hospitalization included a complete hypercoaguable workup, which
showed the following results: Factor II level was slightly elevated at 137 % “normal range being 65120%". The prothrombin 20210A mutation was negative; homocysteine level was 96 (normal range 4 to
10 umol/L); compound heterozygote for the Methyl Tetrahydrofolate Reductase “MTHFR” mutation;
Vitamin B12 was 102 with the lower limit of normal being 200 ng/dl; and folic acid was 2.7 “lower limit
of normal being 5.9”.
Oral replacement for her nutritional deficiencies was initiated and she was maintained on these
treatments as an outpatient.
Physicians need to recognize this potentially reversible risk factor in every gastric bypass surgery patient
who develops thrombosis or thromboembolism.
[Date]
Conclusions: Weight-reduction surgeries are an effective and widely accepted measure of rapid weight
loss. As the population undergoing such surgeries is increasing, the side effects are becoming more
easily identifiable. Vitamin deficiencies, being a known side effect of gastric bypass surgery, may be
preventable with oral supplements and subsequently may have a previously underestimated impact.
The patient's compliance and education are mandatory in such circumstances in an attempt to prevent
fatal complications such as multiple venous thromboses and embolization occurring as a result of
vitamin B12 deficiency.
351
OHIO POSTER FINALIST - CLINICAL VIGNETTE Jason V Kunz, DO
Levamisole – an Emerging Public Health Threat
Jason Kunz D.O., Ben Stewart-Bates B.A. Candidate, Courtney Thomas D.O., Nick Detore M.D., Michael
Rich M.D., Lynn Clough Ph.D.
Introduction: Levamisole is an immunomodulatory agent previously used as both an antirheumatic drug
and adjuvant antineoplastic agent. Levamisole's physical similarity to cocaine allows its use as a bulking
agent; its properties also enhance cocaine’s euphoric effect. Sixty-nine percent of cocaine in the United
States is estimated to be adulterated with levamisole. Levamisole-induced vasculitis in cocaine users is
being seen with increasing frequency.
Case Description: A 51-year-old female with a history of polysubstance abuse and Hepatitis C presented
with a well-demarcated violaceous and necrotic appearing rash on her bilateral ears and right cheek that
progressed over three days. She had a similar rash on her left cheek two months prior. The patient had
associated polyarthralgias and leukopenia. Cocaine was detected in the urine toxicology. Perinuclear
Anti-Neutrophil Cytoplasmic Antibodies (ANCAs) were detected. Cryoglobulins were negative with
normal C3 and C4 levels. Beta-2 glycoprotein and human immunodeficiency virus antibodies were also
negative. Anti-cardiolipin antibodies were equivocal. Cutaneous punch biopsy performed on the
earlobes was reported as vascular occlusive disease.
[Date]
Discussion: Levamisole-induced vasculitis classically presents with purpura of the ears, nose, and
cheeks. Bullae and necrotic lesions can also be seen. Constitutional symptoms including weight loss,
f